Physiology Notes for Midterm
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Date Created: 02/27/15
Wednesday Jan 8 What s physiology 0 O O O 0 How an organism works How do we get a living being to do the things that it does on a daily basis We need to know ion distributions and how proteins interact The systems respiratory circulatory etc are driven by the small things ions and proteins Physiology is the integration of anatomy chemistry physics and biology How the proteins interact involves chemical reactions How we get our muscles to work involve physics Three critical chemical equations MEMORIZE 0 ATP ltgt ADP Pi energy ATP is our currency to get things done We need a quotjobquot to get us ATP Glucose 02 ADP Pi gtgtgt ATP C02 H20 heat We need oxygen to break down our glucose Put ADP and phosphate to get ATP C02 comes from doing work to make energy We also get water and heat Example walking to class we release heat Ourjob as human beings is to make the most quotcurrencyquot C02 H20 gtgtgt HCO3 H We have this C02 and water and we make it happen because not everything likes water C02 is one of those things that don t like water This reaction aids the transport of a key gas Because we don t like water we convert it to bicarbonate We create another problem H creation acid problem by solving another C02 H creates a pH issue Body Organization 0 O O O 00 How is it put together Basic unit for the body is the cell Each cell has your own DNA Mitosis when cells divide Meiosis is for reproductive purposes only Making a cell unspecialized A speci c cell specializeddifferentiated Redwhite blood skin hair muscle etc Differentiation process going from unspecialized to specialized undifferentiated to differentiated o All cells are different but in similar ways 0 Four categories of cells Cell that are of the muscle category Generate a mechanical force Smooth skeletal cardiac muscle cells Nerve cells they initiate and conduct electrical activity We are electrical beings Epithelial cells they separate the boundary between the inside and outside of us Regulate interactions with environment Can also be considered skin cells Although lungs have epithelial cells we breathe air in and so do reproductive and urinary systems have epithelial cells Connective cells they connect anchor support These cells make sure that the other three do their job Not only skeletal but fat cells blood cells provide support Support not only structurally but in a way that they help a system 0 Tissues O Groupings of similar specializeddifferentiated cells We have 4 different types of tissues 0 Muscle nerve epithelial and connective Ussues 0 You wouldn t say I will take a skin cell 0 In this case it would hurt so you would interact with nerve cells We would make it bleed so connchve 0 Skin is not a tissue but rather an ORGAN Organs Combinations of tissues Different organs differ in their composition Do all four groupings need to be present in an organ Yes 0 Do we need nervous connection Yes we want to tell them what to do 0 We need connective Do we need muscular component Yes to control the size and shape or the organ Epithelial is the only category not necessary with ALL organs because not all organs interact with the outside world ie The heart Functional units are the smallest part of an organ that still does all the work What most organs are they are multiple functional units put together For example a kidney is a bunch of nephrons put together The smallest functional unit of the heart is the heart itself Our kidneys are not running at 100 however we only have one heart always going at 100 and if it goes down then we lost a functional unit We need functional groups for redundancy To continue even if we lose some functional groups We need expansion add more functional groups without stopping the ones currently working 0 Organ systems Organs with the same common functions Circulatory system heart blood and vessels Renal system kidneys ureter and bladder Our organ systems can contain other organ systems 0 Cells can t contain other cells and tissues can t contain other tissues 0 For example immune system includes white blood cells the spleen thymus and circulatory system 0 What is inside of us is not all So if all of our cells disappeared we would still be there We wouldn t disappear with the cells Body Organization 0 Fluid 0 Matrix for its function it is a mixture of proteins and minerals to make it up As far as its functions it s like setting up buildings the extracellular matrix is the structure the beams Most important function is to provide structure Extracellular matrices can regulate into transfer How do we make it up 0 Proteins and minerals Extracellular matrices are proteins 0 Main thing that makes up cellular matrix is ber 2 types 0 Collagen ropelike traits They add extracellular matrices to add support The ropelike properties allow cells to move relatively well together When one cell starts to move the other cells will move along with it o Elastin rubber bandlike traits If one cell starts to go away the other cells don t have to move However once a cell stops moving the other cells will come back Like a bounce back effect Non brous not long and thin have a lot of branching o Branching due to associated carbohydrates 0 Fluid componentscompartments Three uid compartments First Intracellular uid cytosol most uid is inside cells Cells are quotsacs of waterquot o In an average adult body 67 of water is intracellular 28 liters Extracellular uid outside cells not second compartment Second Interstitial uid the spaces in between cells actual quotexternaquot For the vast majority of our body is the major environment except for epithelial cells 26 of body or 11 liters Third Plasma uid in blood vessels About 7 or 3 liters How do things move from one compartment to another and what are the boundaries From interstitial to intracellular the cell membrane is the boundary From plasma to interstitial the capillary wall is the boundary That is the wall of the blood vesseL Barriers imit movement How can we cross these barriers to get things to move from one compartment to the other 0 The most important concept of this class is that our body runs on HOMEOSTASIS means quotsame statequot Relatively stable maintenance of a body parameter A synonym to homeostasis is DYNAMIC CONSTANCY Homeostatic Control System Basically a set of interconnected components that are working together to make sure that a particular parameter is where it s supposed to be ie blood sugar Set point is actually inaccurate set range is a better term o For example ideal body temperature is 986 F but everyone s temperature slightly ranges around that area 0 However maintaining this range is important 0 Steady state when we have our parameter at our set point set range when we are at our steady state our system is not going to be changing because we are where we need to be The meals of the day get our bodies out of our steady state sugar spike and our control system will bring it back down to steady state 0 Energy IS required to keep it up at that level 0 Steady state equilibrium Why Equilibrium does NOT require energy no change in energy Because there is only so much energy and energy is limited there are tradeoffs What happens when we are NOT in steady state 0 When something happens to us we can either be reactive or anticipate it and make changes for that For example a person is standing inside a box they can wiggle around range but if someone pushes them off they will come back into the box negative or keep walking away positive 0 Reactive gt response feedback Negative feedback when we have the response be in the opposite of the disturbance The disturbance is raising the glucose the response is lowering the glucose Positive feedback continues in the direction of the disturbance We expect negative feedback of our bodies Proactive gt preparation feedforward FF 0 Limits the degree of feedback required O 0 Less energy required Our bodies anticipate that we will feed out bodies glucose it expects that spike and it already knows that it needs to restabilize and will fee sluggish if it doesn t happen 0 Homeostasis continued Re ex arc From stimulus to response 0 Receptor receives the stimulus O Stimulus can be something external or internal 0 The receptor leads us to the afferent going to something pathway 0 Afferent pathway connects receptor to integrating center 0 Integrating center CNS endocrine or other gland 0 It is the decision maker that decides we have this stimulus let s compare it to our set point If we are still in our set point we won t do anything Example hmm we noticed our body temperature went from 986 to 988 it is still an acceptable range so we won t do anything But if it reaches 100 then we will do something 0 Integrating center then goes to the efferent going away pathway to the response or the order to the stimulus If the body has reached 100 then we will engage the sweat glands Control for homeostatic control center via signals 0 There are chemical messengers These chemicals usually travel through extracellular uid Interstitial or plasma Three groups Messenger endocrine aka hormone O O 0 Released by gland or neuron Pathway it moves through plasma Communicates with distant effectors Messenger paracrine O O 0 Released by most cells Pathway NOT plasma interstitial uid through diffusion don t go very far Communicates with neighbor effectors Messenger neurotransmitter 0 Released by neurons nerve cells 0 Pathway also move through interstitial uid more speci cally the synapse Since the synapse is a very small space it doesn t go very far either 0 Communicates with next neighbor neuron or effector How can we collapse these three messengers into only two groups MondayJanuary 13 2013 Control for Homeostatic Control System 0 Chemical messengers mostly travel through extracellular uid Endocrine paracrine neurotransmitter 0 There are situation where we are moving through extracellular uid to get from cell A to cell B that don t t in the three categories above Autocrine a cell messenger 0 Its pathway is interstitial uid 0 Its effector releaser Cytokine special case because of how it travels Uses all parts of extracellular uid interstitial plasma and lymph Can be considered both endocrine and paracrine but not neurotransmitter Cytokines are the messengers of our immune system 0 All cells above travel through EC uid 0 Some are not based on EC uid Gap junctions direct channels between adjacent cells For example walkways between buildings so that you never have to go outside Intracellular uids are used here because you never have to leave the cell juxtacrines juxta nearby To have a juxtacrine connection we need the cells to come in contact to each other for them to communicate It is bound to a cell membrane For example instead of saying hello you can do a high ve or handshake The contact is the juxtacrine No contact no message sentreceived Contact is made message is sent cells separate messengers stay in their original cells Longterm regulation of the Homeostatic Control System 0 Adaptation Ad traits that favor survival In order to change power to adapt we need to change our DNA Adaptation is something that happens at the species level Adaptation doesn t happen at the individual level What is it that made us want to walk in hoodies in 40 s weather and coats in 20 s weather 0 Acclimatization Ac resetting our set points We are adjusting our physiologies what proteins are present what concentrations etc It is purely usebased NOT genetic It is how we work with the DNA already given we do not alter it If the environment changes we make an adjustment to make us more comfortable to that temperatureother environmental factor Usually it is reversible For temperature we can get used to a colder temperature and then reverse it to a warmer temperature The exception to all of this is DEVELOPMENTAL ACCLIMATIZATION Fetal alcohol syndrome you wouldn t see a pregnant woman taking shots because the alcohol would completely mess up the baby s developmental system We cannot tweak the genetic side but we can tweak our systems to adjust to different environment Adaptation is change in genetics acclimatization is no change in genetics but a change in the environment 0 Biorhythms Body temperature is lowest when we sleep We grow when we sleep They are a combination of feed forward adaptation and acclimatization Adaptation because we can switch if we need to for example third shift workers that have their shutdown time in the daytime We adjust to the different times that the sun goes up and down How can we do this feed forward mechanism How do we adjust to the sun lasting longershorter o If we were locked in this room with no sun exposure we would still be tired at nighttime Reason why is because we are proactive rather than reactive We have an internal trigger that tells us approximately what time of day it is Reactive would make us dependent on looking outside 0 We have a mental clock that tells us quothey the sun is coming up we should wake upquot 0 We adjust to jet lag a little more slowly but that requires a little more reactive than proactive so that you can tell your mind that it is not the right time to sleep A subcategory biorhythm is the Circadian o It is a 2526 hour clock which we make adjustments to If we were locked in we would keep a steady circadian rhythm but it would slowly lose sync to the outside world Annual rhythm we historically put on weight in the fall Once it s spring we diet because physiologically all of that food is going to make us more insulated making us hotter Lunar rhythm we are talking about the pattern to the moon We know the difference between a full moon and the moon not being out When it comes to activities we are more active during a full moon compared to no moon because of our internal lunar cycles Subcellular Composition 0 lons they are important along with proteins in how our bodies work lons have a charge associated AKA electrolytes That charge can either be positive or negative 0 Positive cation Ca2 H Negative anion Cl39 0 Free radical they are important because they change the number of electrons that are present They have a single e39 in an outer orbit and will try to pair up with any other single electron Usually they will take it away from another compound This process of removing an e39 from another oxidizing Receiving another e39 reduction We intentionally make free radicals because the immune system can make them around pathogens the free radicals removes electrons from pathogens and damages them very effective Considered nuclear because we can have them attack pathogens but they are also indiscriminant By that we mean that it will also remove electrons from healthy cells 0 Once our body is healthy again we need to neutralize get rid of oxidantsfree radicals via antioxidants o Antioxidant donors vitamins A amp D 0 Free radical examples 0 Superoxide anion 02 o Nitric oxide NO o Hydroxyl radical OH 0 Molecular bonds how do we keep ourselves together as one unit Covalent bonds sharing of electrons Sharing is not always equal That is why we have partial positive and partial negative charges 0 Partial positive and partial negative charges brings the terms 0 Polar vs nonpolar 0 Polar is nonequal sharing and nonpolar is completely equal sharing 0 Water and oil lipids and fats example 0 Polar vs nonpolar hydrophilic vs hydrophobic o For oil lipophobic fathating is polar vs lipophilic fatloving WednesdayJanuary 15 2014 Subcellular Composition cont Molecular bonds covalent 0 There are basically two categories Polar hydrophilic and lipophobic are all synonyms Nonpolar hydrophobic and lipophilic are all synonyms Amphipatic one section of a compound is polar and one section is non polar One section is hydrophilic one being hydrophobic Like an amphibian this type of compound can be in both land and water Polarity all goes with the quote quotlike dissolves likequot 0 Polar things will dissolve in polar solutions 0 Polar does not associate itself with nonpolar Covalent bonding will usually take some energy very strong Molecular bonds noncovalent lonic electrical attraction of opposites Opposite charges attract each other amp Bond lonic bonds are strong without water It begins to dissolves and breaks apart when introduced to water 0 O o If you put an ionic bond inside a person the water will dissolve it and break it apart 0 HYDROGEN BONDING interaction with bound hydrogen The cohesiveness of water creates surface tension as water molecules hold on to each other via hydrogen bonds No two water molecules ever stay constant The partial charges force them to constantly move 0 HYDROPHOBIC Nonpolar interactions avoiding polar Water and nonpolar don t like each other and nonpolar molecule will avoid the water or any polar environment Weak association Easy to break apart SECTION 28 Plasma membrane 0 Functions cells are cells because they are isolated They each have a membrane that separates intracellular and interstitial Plasma membrane regulates movement in out within Binds chemical messengers Holds cell in extracellular matrix Allows for cell s shape and motility Our cells won t be just spheres Allows for cellcell contact SECTION 38 0 Components that make up the membrane are in uid mosaic form Main building blocks are phospholipids Phosphorus fatty lipid Phospholipids have a bilayer they each have a polar head and two nonpolar tails The polar heads face the outside and the nonpolar tails are on the inside of the membrane Polar head and TWO nonpolar tails Phospholipids are AMPHIPATHIC Completely based on the fact that their nonpolar tails are trying to avoid the rest of the water inside us they form spontaneously Imagine you want to build a house You go to Starbucks and when you get back it s already built 0 It phospholipid builds itself with little energy 0 Cholesterol Necessary for our bodies Amphipathic they lie inside the membrane with the phospholipid tails and with the heads They need to be in our cells so that our cells can form vesicles 0 Proteins two categories Integral proteins 0 They serve as channels to let things in and out of a cell They also serve as receptors They receive messages and interact with endocrines paracrines and neurotransmitters We need to connect our membranes to other cells and extracellular matrix they serve as anchors 0 They are Amphipathic and not removable If you pull out a protein that is attached to the membrane it will damage not only the membrane but the entire cell 0 Many but not all are transmembrane going across the cell membrane Basically they have one side exposed to the intracellular and one side exposed to the interstitial uid Peripheral They impact shape As we change the shape of the protein we can change the shape of the membrane 0 They also set up whether the cell will be able to move 0 Peripheral proteins are most typically polar They are located on the inside surface the cytosolic side 0 Glycocalyx cell metabolism Allows for identi cation and interaction of cell with other cells The Glycocalyx in person A s cells are different that person B s cells They are short branched carbs Those branches give a fuzzy surface when observed under a microscope The fuzzy stuff is outside the cell the clear is inside the cell 0 JuncUons Associations junction together Cells of the same type make tissues Junctions are all about interactions between cells in order to make tissues Example 1 gap junctions 0 Channels linking two cytosols This is a way for stuff to move within intracellular uid Not an endocrine paracrine or neurotransmitter These are small so only limited exchanges between cells 0 They still allow for interstitial uid to ow between two cells Literally in the space between GAP JUNCTIONS ARE LIKE WALKWAYS BETWEEN TWO BUILDINGS GO FROM ONE PLACE TO ANOTHER WITHOUT GOING OUTSIDE Example 2 Desmosome protein linkage between cells 0 Spot welds like a spot of Velcro chewing gum stuck between two basketballs to hold them together 0 We know that we are not going to have intracellular ow But there is interstitial ow Example 3 tight junction joining of plasma membranes This blocks interstitial uid FridayJanuary 17 2014 Cellular Metabolic Pathways 0 When we look at our cells our currency is ATP Adenosine Triphosphate o Phosphate bonds are high energy ATP ltltgtgt ADP P E Equation 1 Triphosphate becomes diphosphate and another phosphate 0 How do our cells make ATP Substrate Level Phosphorylation Bound Pi phosphate transferred to our ADP ATP X ltltgtgt ADP XPi Example glycolysis 0 One of the ways that we make ATP 0 Example Krebs cycle 0 Example Creatine in muscles Oxidative Phosphorylation o It is set up by the Electron Transport System 0 Energy input allows unbound P to bind ADP Our equation 1 with no additions necessary o ETS is the only way of making ATP via oxidative Phosphorylation o Glycolysis breaking sugars down Start carb catabolism Series of 10 NZ reactions enzymatic An enzyme is a protein One of the most important categories of proteins Anything ending in ase is an enzyme They help a reaction happen but don t get used up in the reaction allowing them to be used more than once 0 Example TA s are enzymes They can help one student without then forgetting the information They can help another student afterward Location cytosol Net production 2 ATP Glycolysis makes ATP via substrate level Phosphorylation and it makes 2 ATP for every sugar glucose you start outwith You get other stuff too You get some Hs Our third product will be variable dependent on what is happening around that cell o If the cell is in aerobic conditions will make pyruvatepyruvic acid synonyms Aerobic conditions means oxygen is present o If the cell is in anaerobic conditions glycolysis will still happen you still get 2 ATP s Hs and LACTlC ACID lactate Oxygen present pyruvatepyruvic acid 0 No oxygen present lactatelactic acid Regulation when do we do more and when do we do less o If we have a lot of ATP more money than bills a high concentration of ATP you won t run glycolysis which then runs glycolysis less o If you have a lot of ADP more bills than money 0 This will get our glycolysis to happen more in order to make ATP So our ATP is produced but what about our Hs and pyruvatelactate It moves into our Krebs Cycle 0 Krebs Cycle AKA Citric Acid Cycle or Tricarboxylic Acid Cycle This is a cycle process so it keeps feeding back into itself It needs a starting point typically pyruvate from glycolysis Not always sometimes uses protein and fat catabolism products Series of 8 NZ reactions Location this ONLY happens in the mitochondria Any cell that doesn t have mitochondria only has glycolysis Net production 2 ATP Byproducts H C02 0 The 02 is needed indirectly in order for Krebs cycle to run If we take away oxygen it will shut down 0 To recycle coenzymes Regulation same as before A lot of ATP present Krebs cycle shuts down Lots of ADP Krebs cycle cranks it up 0 Electron Transport Chain Start H and CoNZ coenzymes Location mitochondria Net production 34 ATP 0 From Phosphorilation It s not just about ATP We also get H20 and recycled coenzymes The Krebs cycle is dependent on the Electron Transport Chain 02 is directly required in the equation and the end step of reactions Krebs cycle is Indirectly dependent on oxygen without oxygen it would not be able to run Note instead of H20 coming out of our electron transport chains we can produce 02 and OH radicals Refer to FIGURE 346 C6H1205 602 Pi gtgtgt quotHzO 3438 ATP 0 This generates HEAT 0 How do we transport things across the membrane so that we have some things inside and some things outside the cell Membrane transport 0 Unaided movement depends on Size there are small things that can sneak through it the smaller the easier to get through the membrane Charge nonpolar not charged are easier to get across Small and nonpolar can pretty much get through effortlessly The larger and more polar will be harder to get through Protein channels and transporters 0 Function regulate transport 0 Example by regulating the fence the tiny dog can get through the fence 0 Those examples tie into the concept of DIFFUSION Diffusion happens in nature all the time Creates movements of compound from their high concentration to their low concentration Diffusion gets oxygen and other compounds into our cells via diffusion Our bodies are extremely dependent on diffusion Dependenton o Permeability if we increase the permeability the rate for diffusion will increase Permeability is a direct relationship 0 Direct relationship if we were to graph the diffusion rate against permeability as permeability gets higher it also gets higher So by direct relationship it also means positive correlation Surface area direct relationship As surface area goes up diffusion rate also goes up 0 Concentration gradient what s the difference between two different areas that require diffusion Also a direct relationship 0 Distance It is not direct but inverse The farther you are from the permeable membrane the slower the rate of diffusion Opposite Diffusion simply takes things from areas of high to low concentration When it comes to the inside and outside of a cell there is diffusion through a lipid bilayer It doesn t need energy to diffuse Small and nonpolar things can move through 02 and C02 The barrier in our membrane is not a membrane for oxygen o This is a problem because we want to STORE oxygen However there is no 02 storage in cell because it diffuses to outside the cell We could diffuse through the protein channel AKA Ion Channels 0 Things can go both in and out o Gating what can switch us from opening and closing the gate 0 Ligandgated ligand binding to channel 0 Voltagegated change in electrical distribution Example hair and static electricity 0 Example between ligand and voltage Ligand is like having a key to open a car voltage is like having a button and doing it electronically o Mechanically gated we know our plasma membrane is always moving If we pull on our protein we can stretch it or move it to cause it to mush together For example our bladder opens and expands Another example is someone using a crowbar to get into someone s car 0 It s not just ions that move through these channels special case 0 Aquaporins water that goes through the channels Channels that allow water to move Osmosis the process of how water moves through these channels Osmosis diffusion of water through protein channelmembrane 0 Water will move from its high concentration to low concentration of water which means it goes from areas of low solute concentration to high solute concentration refer to gure 416 0 This measurement is called OSMOLARITY o Osmolarity is the total solutes in a solution 0 A concentration is x of xvoume o 3 mol of Mg2 2 mol glucose in 1 L what is the Osmolarity Answer 5 Osm o 3 mol of MgClz 2 mol glucose in 1 L 11 Osm MgClz is very weak therefore it would completely dissolve 3 Mg 6 Cl 2 glucose 0 What does a higher Osmolarity mean More solutes present If we have more solutes present that means we will have a smaller water concentration Osmosis is NOT the diffusion of water it is simply diffusion o If we take a cell and look at it and put it into a solution the inside of the cell will have an Osmolarity ATP protein etc o The size of cells is impacted by water movement 0 lsotonic same np nonpenetrating solutes outside the cell No impact If we put the cell in an isotonic solution it would not change or be affected 0 Hypertonic higher np solutes outside the cell Osmolarity is higher outside the cell which means the water from the cell will go OUTSIDE the cell making the cell SMALLER o Hypotonic lower np solutes outside the cell Osmolarity is higher inside the cell which means water will go INTO the cell making the cell LARGER Osmotic Pressure 0 Refer to 417 0 When both water and solute are permeable through the membrane there will be equilibrium no problem 0 If only water was permeable but the solute couldn t go through the membrane the water would go through and the membrane would move itself so that there are equal osmolarities based on VOLUMES o If the water could go through but the membrane couldn t move you have a xed space you can t change it The boundary is xed so as a result of permeability to water AND no membrane movement you increase the pressure Volume and pressure are inverses O You invoke osmotic pressure when only water can move semipermeable AND membrane can t move xed in place You have twice the number of solutes and less water in the side with the most solutes but the same volume for both lons and proteins get through protein channels nonpolar items can go through easily Carriermediated transport gure 48 0 The protein is acting like a quotshuttlequot The particles aren t just going through the channel they are interacting with the protein channel 0 The interactions bindings regulate the transfer 0 First Method Facilitated diffusion using the protein to help diffusion o The compounds will move with their 0 O 0 gradient and since its just diffusion there is NO energy cost This is based only on conformationshape changes that cause the protein to move and open into the other direction This can be saturated meaning overloaded When the protein channel is transporting one particle there are others waiting An example of facilitated diffusion is glucose lfl ate a ton of sugar it wouldn t get into my cells immediately but all the sugar will be waiting to be transported Second Method Active Transport 0 0 Almost always against gradient Everything we talk about is based on diffusion Making a gradient does not rely on diffusion so this costs energy This is based on conformation changes Binding things unbinding things etc and ATP There are two ways to do this Primary active transport We will see ATP gets directly used When we look at transport protein 411 we can see the transport protein use the ATP That means we need to use EQUATION ONE Transport proteins ATPase pumps ATP gtgt ADP Pi Sodiumpotassium pump if Na is low inside and high outside it will move Na outside the cell and vice versa For this pump to occur rst the ATP binds this causes a shape change lT doesn t necessarily matter that it is an ATP if it wasn t present however the sodiums wouldn t be able to bind The ATP binds then the 3 Na bind which then causes hydrolysis of ATP ADP Pi E and the P stays That then causes the channel to open to the outside releasing the Na When it is already open the other way and the Na leaves the inside of the channel changes shape to allow the potassium K to get in the channel and go into the cell You release Na gtgt 2 K bindgt then release P gtgt the channel inverts so the opening is inside again and the K is released into the cell Now the high to low of both Na and K has changed and they want to switch sides again 0 Secondary Active Transport uses ATP indirectly Uses the energy in an actively established ion gradient to move a 2nCI molecule against its gradient 0 Cotransport two things that are moving in the same direction sodium and potassium leave together O o Countertransport sodium leaves potassium enters Opposite directions What if we need something bigger than a protein to move stuff in an out of a cell You form VESICLES Vesicle formations are for moving large compounds This requires ATP and cholesterol What does cholesterol do Helps in the bending of that membrane Endocytosis in fold of the membrane The inside of the Endocytosis vesicle contains interstitial uid because it is the uid that was just on the outside is now on the inside 0 Forms intracellular membranebound vesicle If we want to move things OUT of the cell EXOcytosis o The vesicle fuses with the membrane and it releases its contents to the outside Figure 4 20 Functions of Endocytosis 0 Move things from one side of the cell to another Transcellular transport compound X goes in through the cell and exosytoses to the outside Endosomal processing we might be bringing compound X in so that it can meet with compound Y which is already inside the cell to do something INSIDE the cell Destroying engulfed materials bacteria are being endocytosed so that it doesn t damage the cell o If you keep doing Endocytosis will cause the cell to shrink because you keep penetrating the cell membrane because you re taking part of the volume 0 You NEED exocytosis to balance that out It replaces recycled membrane 0 There is a chemical messenger release Recall the re ex arc O O Stimulus gt receptor gt afferent pathway gt integrating center gt efferent pathway gt effector gt physiological response Where are signals being passed Keys Signals messengers ligands Receptors proteins that bind ligands Problem Receptor ligand releaser Effector receptor Our effector will have to have ligands associated with it Receptor has two de nitions 0 Receptor passes message to integrating center 0 A protein that binds a ligand How will we know whether we re talking about the protein or the re ex arc We will be given the right context Receptors o Terminology Activation when a ligand binds to a receptor we are activating the receptor If the ligand is simply oating around with no contact to the receptor there is NO activation The matching has to be complimentary Example ionic plus and minus Speci ty is a yesno answer It is either a perfect match or no match to the receptor Affinity the strength of the binding In example 329 protein 1 is a perfect match with charge and size With example 2 the shape ts but not enough charge With protein 3 there is no correct charge NOR shape 0 The lower the affinity the more likely the connection will break The saturation is the percent activated The curve highest on the graph will match best to the highest affinity Competition Antagonist no response Agonist response 0 When something binds to a protein we get a conformation shape change If something binds to a protein and the response is stopped we have an antagonist If we want to stop a particular pathway 0 For an agonist we get the opposite we get a pathway to proceed Activation of our receptor converts our signal into a response 0 Signal transduction pathways If our integrating center is sending something to our effector then we should have the right thing going INTO the integrating center Signal transduction is how cells communicate so that then we can use that communication to adjust the communication when it s not doing what it s supposed to be doing in someone s body Signal transduction is the message going from outside to inside the cell Activation is simply the rst step into cell What are possible responses that we might see in a cell 0 A change in the membrane of the cell 0 We might want to change the membrane for movement across the cell membrane 0 Example transport of insulin changing membrane to allow transport proteins to leave or stay 0 Alter metabolism focusing on glycolysis We need to focus on the mitochondria to produce more ATP The Krebs cycle could be told quothey we are running out of glucose switch over to the fat and start burning that for more energy 0 Change in contractile activity Secrete product endocrine system glands receive message to release a particular endocrine Product could usually be about releasing another signal 0 Change in proliferation or differentiation rate This is the time to make more cells that look just like you proliferation or this is the time for you to start going to a particular pathway and for you to become a specialized cell differentiation Where do we see our various receptors Locations Intracellular within cytosol or nucleus Membrane bound our receptors are on the surface 0 With these two categories we look at them individually to see what information we know aboutoungand Intracellular 0 Within nucleus or cytosol o If it is inside the cell it has to go from cell A to cell B and to get to the receptor it needs to cross the membrane which means that the ligand wouldn t be easy and in order to cross the membrane without any help it needs to be SMALL and NONPOLAR If the ligand is nonpolar you need a plasma binding protein If what you are transporting is NONPOLAR but the medium in which it travels is POLAR you need a plasma binding protein The plasma binding protein HAS to be AMPHIPATHIC Ligand receptor COMPLEX The complex has to be in the nucleus Once the ligand binds to the receptor the complex is present in the nucleus If it all happened in the cytosol it would move into the nucleus The response has to be in the nucleus because that s where the DNA is The complex will react with the DNA and the result of the activation of an intracellular receptor wi ALWAYS going to get a change in how the DNA is worked with o The ligand binding to the receptor will impact how the DNA is read The DNA might get read more or less Membrane bound receptors 0 O O 0 Two types of protein integral or peripheral This one in gure 55 is integraltransmembrane protein Ligand will be POLAR which means that it will not be able to cross the membrane Ligand poar no entry The ligand cannot enter the cell unless there is a protein present to allow it into the cell The protein HAS to be integral and transmembrane In a relay process it is the rst but there will be a second and sometimes even third and fourth involved Four categories Receptor is functioning as an ion channel Ligand gating a ligand caused the channel to open 0 The result is an in charge distribution Function as an enzyme tyrosine kinase 0 Anything where kinase is involved requires the FIRST EQUATION The result is a cascade of phosphorylations For last two categories the receptor is the middleman and more steps are required Interaction with a JAK kinase 0 Kinase EQUATION ONE phosphorylation will happen o The result is the new proteins to synthesize Interaction with a G protein 0 Heterotrimeric it is the most common and complex of our systems Most commonly used in our bodies 0 When G protein gets activated that shape change allows the alpha subunit with GTP most of the energy in our body is done by ATP but we have GTP ATP as well 0 When it does that it interacts with plasma membrane effector protein PMEP It is an integral transmembrane protein Can be either ion channel or enzyme 0 Example includes adenylyl cyclase gtgt cAMP Using this as an example shows one of the cases not the ion channel if we open an ion channel we will change our charge distribution this is an enzyme example Keys to remember with this for every one messenger that s binding to a receptor it will interact with one G protein interact with one adenylyl cyclase and produce several enzymes depending on the ATP available The cyclic ATP will activate other enzymes Enzymes do EQUATION ONE Any time in physiology like in this example where we have an enzymatic process we amplify meaning that the enzyme can do its job more than once Anytime we have an enzyme we multiply the production In terms of cyclic AMP being made by adenylyl cyclase we end up seeing every single one of the responses that we mentioned were possible to happen when the receptor is activated can happen here 0 We could change the membrane 0 Change the protein channelstransporters present 0 In terms of changing shape our microtubules will impact that 0 Release something else 0 Change the metabolism 0 Switch over to lipids get a storage component of glucose which is then broken down Colligeration o All of these responses happen from just ONE ligand binding FIGURE 59 0 Receptor Activation We need to NOT have as much communicationdecrease the communication by releasing something that can damage the ligand before it nds the receptor 0 One way to decrease this is by going after the messenger by catabolizing it not allowing it to get close enough 0 We can also just go after the receptor To lower its likelihood of interacting with the ligand is by lowering the af nity we make it harder for it to be able to bond If we lower the af nity to zero then we don t have binding possible elimination of speci ty We can also make it harder for the ligand to associate with the receptor In other words hide the receptor 0 The polarity of a ligand for a membrane bound receptor is polar and a polar ligand CANNOT cross the membrane polar cannot go through nonpolar region 0 In terms of this idea when talking about membrane bound receptors we will ENDOCYTOSE them this hides them so that they can cross the membrane Turn off a phone and you won t get messages turn it back on and you will get the messages 0 Another way is by going after one of the SECONDARY MESSENGERS The most common way to disrupt that process is not by going after the ligand g protein adenylyl cyclase but rather by going after the CYCLIC AMP When cyclic amp gets made it gets broken down so that it doesn t activate the enzymes o If we want to INCREASE the communication Put more receptors out there in order to increase likelihood of receptors receiving the message 0 This can be done if talking about membrane bound receptors via EXOCYTOSISanabolize opposite of catabolize or basically making upmaking more of something Nervous System O O O O 0 Central CNS brain and spinal cord integrating center in terms of the re ex arc anything encased in bone is CNS Peripheral composed of efferent gathering info and afferent getting activities caused Afferent is sensory nervous system Efferent is what controls muscles getting glands to do their work etc Overall what do we need accomplished by nervous system The slower way to communicate is the endocrine system much slower We need to start with the smallest unit Neuron AKA nerve cell FIGURE 61 Anatomy of a neuron Cell body central part contains the nucleus The arms coming out of the cell are the processes 2 categories The DENDRITES smaller arms are ways to connect to other cells They get information from other cells and communicate inputoutput processes oVarious neurons can have upwards of 400000 dendrites each 400000 potential connections being made with other cells Dendrites gather information from other cells speci cally gathering neurotransmitters Neurotransmitters are the way they communicate with each other 0 Communication could also be environmental stimuli bang the back of your head and seeing stars comes from impacting neurons Why so many and why are the ends branched To increase surface area The higher the surface area the higher the likelihood of better communication More surface area gives the opportunity to put more receptors out there so that if a ligand needs picked up there will be a receptor waiting to pick it up The AXON long single arm is referred to as the quotnerve fiber 0 Axons can sometimes be up to a meter long 0 O Lou Gehrig s disease has to do with the axons broken down and the pathway being lost oThe axon delivers information It sends out the message that the cell needs to communicate with the additional cell 0 Axon terminal at the very end of the axon furthest from the cell body This releases neurotransmitters The largerlonger it is the more likely that it will increase the axon s communication capacity oThe branch coming off the side of the axon is the COLLATERAL We can have multiple collaterals branching off the axon The collateral allows the expansion of even MORE information 0 Myelin Composed of several layers made of plasma membrane The axon does not have multiple layers The structure around it is NOT the axon itself The thick layer of plasma membrane is actually created by other cells that are taking their own plasma membrane and extending it and wrapping it around and around the axon In other words the myelin comes from other cells Plasma membrane is originally the membrane differentiating the inside and outside of the cell Now we have several layers which then dramatically decreases the likelihood of anything leaving The thick layers provide insulation to the cell to protect the information from the outside Our neurons generate electrical signals In the PNS we have what are called SCHWANN cells 0 Each Schwann cell wraps around the axon They make myelin and only do so in the peripheral nervous system and they only cover PART of the axon not the entire thing In the CNS instead of SCHWANN cells we have o OLIGOCENDROCYTES They can cover several axons unlike Schwann which only covers one and are ONLY in the CNS You don t want complete insulation around the axon Nodes of RANVIER You want small gaps between the Schwann and Oligodendrocytes These nodes expose the axon to INTERSTITIAL uid 0 CNS Composition Neurons Glial cells AKA neuroglia Glial cells exist because they support and help 0 Physically and metabolically they provide support for the neurons They are the CFO and vice presidents to the neurons CEO They are ONLY in the CNS Neuron to Glial cell ratio there are many more Glial cells per neuron In terms of the nervous system 90 are Glial cells but only 50 of the total volumes in nervous system since the neurons are so much bigger Different types of Glial cells 0 Oligodendrocyte covers multiple parts of multiple axons Microglial macrophagelike cell Macrophage like a cell that eats other cells cells are associated with the IMMUNE system Microglial serve an immune function This is important because when talking about cytokines they move through plasma interstitial uid lymph etc immune system moves through the same place Ependymal cells they tie in with microglial cells They line the cavity that creates the CNS Extracellular uid but they have two different compartments One of these compartments contains cerebrospinal uid It helps make sure that we have the right amount of uid in our cerebral compartment Astrocytes regulate extracellular composition These appendable cells are creating a boundary inside our CNS separate from the interstitial uid in our body They help regulate composition by removing K and neurotransmitters If we got the message transmitted we want to get rid of the messenger Astrocytes help with that They also stimulate tight junctions in capillary walls They wrap around capillary walls to make sure that the tight junctions are working properly and that no viruses or anything are getting in there Astrocytes also have arms that wrap around neurons They provide metabolic support with glucose and ammonia The ammonia oThey are very critical in neuron growth 0 Signal system Different types of neurons three categories 0 Afferent they bring information TO somewhere Carry information from our receptor unless afferent neuron IS the receptor Parts in the PNS are the cell body most of the axon Parts in the CNS are the small axon o Efferent sending information out to the effector muscle gland other neuron etc Parts in the PNS include the majority of the axon but the cell body and dendrites will be in the CNS 0 lnterneurons they do the connection creating relays between what afferents bring in and what the efferents bring out Everything about them is inside the CNS 0 For every one AFFERENT you have ten EFFERENT neurons and 200000 interneurons 110200000 How do we get our neurons to talk to each other Synapse 0 Electrical fastest Happens through gap junctions lt s two way 0 Chemical slower lt s oneway It s a little slower but it always goes to the destination Presynaptic and postsynaptic What s between the synapses Interstitial uid Convergence and divergence We all converge for class in the morning and diverge after class and go our separate ways 0 Convergence pre gt post Divergence pre lt post How can our cells be electric Membrane potential oThere is electrical charge separation across the Plasma Membrane due to distribution of charged components 0 Electrochemical gradient most cells are slightly negative on the inside For example sodium is high on the outside and low on the inside which means that it is more negative on the inside Concentrationwise that means that it s going to move in 0 Net G conc G elec G One will dominate Will potassium go in or out Membrane potential 0 Measure of voltage gradient VM voltage across membrane at rest most cells are at 70 VM 0 When we do this this will be the result of all charged components What s underlying all of the and charges is the distribution of sodium and potassium VM 2 Ex of all ions Ex is the equilibrium potential I VM ENa EK ch etc 0 Similar to Osmolarity is the sense that we do this based on the sum of the concentration gradient V at which elec And Concentration Gs for a component are balanced o How do we change our VM We alter the plasma membrane permeability You increase permeability ions move causing change in VM which then yields the graded potential Only happens as soon as we have a change in membrane potential We don t talk about graded potential unless we are talking about changing our permeability We will see the most change close to the ion channel and less of a change the further you are from the ion channel 0 Looking at a graph xaxis is time and yaxis is membrane potential Our cells are POLARIZED at rest Remember becoming less negative is going towards zero because at rest the number is negative 70 This process is called DEPOLARIZATION When you are depolarizing the cell you are stimulating the cell The opposite is becoming polarizedmore negative and when something becomes too polarized the term is HYPERPOLARIZATION When you hyperpolarize you are inhibiting the cell If we want to return our cell to rest you REPOLARIZE 0 Characteristics to look for A stimulus is anything that impacts the cell Two terms of stimuli for when hyper or depolarizing When we see a small stimulus that creates a small graded potential A bigger stimulus gives a bigger graded potential The bigger the stimulus the biggerstronger the signal that is better for communication However graded potential is local so as we get further away our size gets smaller As our signal also decreases with distance we have a problem What happens if our graded potential occurs near a voltage gated channel Voltage gated changes the distribution of electrons All we need to do is change the membrane potential graded potential So we need a graded potential of the right size to open a voltage gated channel In excitable cells the graded potential can cause a very large change in our VM All cells in our body can and will have graded potential Only excitable cells will have action potential To get action potential Either we have one happen and it looks excitable or we didn t meet the conditions and nothing happens There HAS to be enough pressure to create something What components do we need to have the special type of graded potential to have action potential We need voltagegated channels present 0Voltagegated channels that allow sodium through them Basically you have an extra protein inactivator that when you are close to being open when we have the right distribution of electrons that causes the gate to open that change also causes the protein to start moving oven Second kind of channel is voltagegated potassium cells Events of an action potential how do we get this large quick change in our VM We start with membrane at rest 70 mV 0We need an action potential that causes a depolarization it needs to go up more positive Once you go up you will reach threshold potential Once you get there you will have what you need to open the voltage gated sodium channels What When ourth Sodium goes in but are we changing our VM Yes we are moving plus charges inside which causes the VM to become more positive oThis causes an in ux of sodium which cause more of a depolarization Our stimulus causes a depolarization the cell s response is to cause more depolarization POSITIVE FEEDBACK It needs to stop eventually however Eventually our inactivators wi swing over to stop it inactivates sodium in uxsodium channels What is the difference between being closed and inactivated lmagine just getting home and opening your garage you go in and that s it But if someone is blocking your driveway that car is the inactivator preventing you from going in your garage Anyway when the in ux is sodium is stopped the potassium channels open Will the potassium in ux or out ux 0 Where does potassium want to go Toward lower concentration which means outside which means it will OUTFLUX Potassiums leaving the cell will cause the VM to start going down which means it will start REPOLARIZING again Because the cell is slow to close we overshoot our resting potential which means that the cell will become more negative than it is at rest causing HYPERPOLARIZATION The threshold by de nition is the VM required to activate our sodium channels happens when we have a weak depolarization we see a stimulus but it s not enough to reach reshold potential You get subthreshold potentials AP amplitude AKA size if occur Independent of stimulus No change in size GP Practical application Many local anesthetics go after impacting those voltage gated sodium channels When we saw our inactivator moving to deactivate those sodium channels they would make sure there was no in ux of sodium Many local anesthetics block Na channels Action potentials AP Propagating down the axon Adjacent sections of plasma membrane oThere is no movement One starts the next We have our rst section getting our action potential That graded potential is the trigger that causes the next reaction and it essentially causes a chain reaction 0 As distance goes up we just have more action potentials in our chain But we don t see any change in the size of the action potentials There is no decrease like the grade potentials With this in mind there is no signal present Distance becomes irrelevant as long as we have the axon covering it with the action potentials Unidirectional chemical synapses are unidirectional The process of triggering the dominos to fall over action potential chain reaction has to go all in the same direction How do we keep this from going in multiple directions There are two key things The rst one is the hyperpolarization They were slow to open and also slow to close causing a lot of potassium to leave the cell overshooting the resting VM When an area is still hyperpolarized it is subthreshold Sodium channels are blocked inactivated Even when we get above threshold the inactivator is still in place causing no sodium in ux therefore there is no action potential What do we know about axons Myelin Most of the axons in our bodies have myelin associated with it What are the sources of myelin Oligodendrocytes or Schwann Myelin serves as an insulator protecting the electrical IO 0 IO component not allowing to be dissipated to the environment like the wires in our house Myelin aids graded potential What causes the drop to go faster or slower Myelin is layers of plasma membrane Will ions like K and Na be able to move No Myelin aids graded potential but it blocks action potential Myelin helps increase the conduction velocity For every action potential it would take 2 milliseconds which could potentially take a lot of time for the action potential The graded potential is faster We need the action potential to happen but they happen at the nodes of Ranvier In the sections covered in myelin you have graded potential and the open sections are action potential This is called salutatory conduction It looks like a jump over the myelin but in reality it buries itself and emerges This jump to the next node is done via the graded potential If we take away the myelin we start having problems because we start slowing things down and if we don t get the channels to take over the area we can actually lose the message being sent or it will never reach threshold potential Back to chemical messages We can have many inputs from many pre synaptic Multiple pre synaptic can impact one more post synaptics is called convergence 0 Excitatory depolarizing it will make it more likely to have an action potential and get us to threshold Inhibitory hyperpolarizing We need to get it up to rest rst and then that means it is less likely to have an action potential occun 0 Temporal summations If we take the input from A and we don t do anything with the cell it will return to rest But instead of going to rest A hits it with another message so it will build off wherever it was One Presynaptic hitting the postsynaptic in time Spatial summations O Gives us the same kind of depolarization as A but what if two presynaptics A amp B hit it at the same time It just looks like one big input rather than two smaller ones hit it The more presynaptics we have the more ways we can put them together so that we can reach a threshold potential 0 Synapses can change info and the more we have the more complex Synapse strength how likely it is that we will pass the message from cell A to cell B There are things we can do in terms of cell A and things in terms of cell B to get a message across If it is a chemical synapse we need a neurotransmitter If we don t have one we need a ligand or else we won t get the message across Calcium availabity is critical to actually having vesicles get exocytosed We need calcium to be able to move into presynaptic neuron to be the trigger that causes exocytosis Receptor availability ask party room Membrane potential less likely to pass electrical message if hyperpolarized Postsynaptic factors 0 Receptor availability have to be able to bind Hgand 0 Membrane potential depolarization makes it more likely Anatomy of the Brain 0 Cerebral cortex also known as the cerebrum It helps us perceive the world Five people can witness the same event but you can get ve different stories Perception is a ltering system based on what each person puts more focus in It allows voluntary movement Language understanding what is being said To be able to have language we need to have learning memory It all happens here Gray matter the outer shell Cortex means quotouter partquot What is creating the gray area is clustering of cell bodies Why are brain injuries such a problem Because the important parts are right on the cortex Clustering of cell bodies nuclei In respect to the nervous system we re talking about clustering of neurons White matter inner layer 0 This is where we see our axons running Oligodendrocytes creating myelin wrapped plasma membrane a whole lot of phospholipids are white 0 Ventricles There are 4 chambers In the heart chambers are lled with blood In the brain they are lled with uid Those are areas that help regulate interstitial uid This is an area where we have containment of it 0 Corpus caosum Connects left and right halves of the cerebral cortex Massive bundle of axons Why is this there To allow for communication of the two halves Connects two hemispheres o Diencephalon includes thalamus and hypothalamus Thalamus it used to be that this was the area that controlled movement It still has the capacity to control your movement So all our movement that is voluntary was controlled by the thalamus Additionally this area is involved with crude sensation We have seeing hearing area and more things to give us detailed information about the world around us This is also the area associated with REFLEXES Picks up on crude sensation of a fast movement before the cerebrum could pick it up The cerebrum is what recognizes something is being thrown at you Hypothalamus this helps us in terms of maintaining homeostatic control systems How so We need stimulus info from nervous system via endocrine system This is the link between nervous and endocrine systems 0 Forebrain combination of the cerebrum and diencephalon o Cerebellum is about being able to take muscular activity and control and be able to coordinate it Balancing activities It impacts our muscle tone and overall our coordination Being able to put patterns of muscle movements together in a coordinated way standing on one foot Little kids haven t fully engaged their cerebellum hence them not being able to walk 0 Brainstem the very end of the spinal cord Even before we were running things off the diencephalon we were running things off the brainstem The most primitive things in terms of us being alive are controlled in the brainstem The key to life It is responsible for us breathing having a beating heart digestion O Spinal cord In terms of digestion we don t want to damage the respiration part When we get stuff to our stomach the brainstem makes sure our airway is protected and that food doesn t go to our lungs Same with vomit We don t want vomit to go into our lungs gray area and white area Gray area in the middle and center inside the spinal cord reverse pattern of the brain cerebrum In the brain 0 White Anatomy of the o O the gray area is on the outside Interneurons we have cell bodies and dendrites of efferent neurons communicate with interneurons Axons of afferent and Glial cells are in the gray matter matter myelin Bidirectional two way street Components come out on one side and go in on the other The dorsal side is the afferent The ventral side is the efferent Why is it important for the afferent outside If we re getting damaged from the back in this situation we will lose sensory rst You prefer the ability to move over the ability to feel So the side related to sensory afferent is dorsal so the part that is related to motor efferent is more on the inside However damage from the inside will affect motor rst Basically if you damage the white matter you won t get the message telling you that you need to run If you damage the gray matter inside you will get the message that you need to run but you physically won t be able to DAVE PNS Spinal nerves exit via the vertebral column Cranial nerves exit via the skull openings O O O Clustered cell bodies in the PNS are NOT nuclei rather they are called GLANGLIA Grouped axons big connection points in our limbs Pathways or tracts example shoulder is the connection point from all the nerves in the hand and forearm Groupings of axons are called nerves Big groupings are called pathways or tracts Key neurotransmitters Acetylcholine ACh at the synapse where this is use Achesterase is an enzyme that breaks down any ACh coming toward me Why does it destroy it The idea is that we want this message to be distinct coming off Cognition a lot of the stuff happening in the cerebrum communication is happening with ACh Same with behavior and getting glands to work Also with getting a lot of organs like muscles to work are told what to do by ACh Biogenic Amines Dopamine norepinephrine serotonin histamine A lot of this will happen in the brain stem and hypothalamus Involved with consciousness mood and endocrine regulation Amino acids Excitatory vs inhibitory depolarize vs hyperpolarize Proteinde cient diets can affect you because of a lack of amino acids Neuropeptides peptides are simply short chains of amino acids that aren t quite proteins yet Two or more amino acids changed together can be called a peptide They also act as endocrines and paracrines Nervous system Central is brain and spinal cord and sends to peripheral which is made up of efferent and afferent Efferent is made up of autonomic and somatic Autonomic is made up of sympathetic and parasympathetic On the efferent side you control things in two ways 0 O Autonomic think of it as automatic Has CNS controlling things without you requiring a lot of thought For example our heart and breathing Somatic what we do in terms of voluntary control using our cerebral cortex Both send signals from CNS to effector cells Figure 646 oThe somatic only has one neuron whereas the autonomic has TWO neurons going to the effector 0Somatic innervates skeletal muscle and nothing else Autonomic innervates 0 Smooth muscle cardiac muscle glands GI neurons involved in the digestive tract 0Somatic only excites whereas autonomic excites AND inhibits 0 Purpose of autonomic nervous system Regulate automatic visceral responses How does it do this Two opposing systems gasbrakes 0 Sympathetic vs parasympathetic Both innervate most effectors We end up seeing a cluster of cell bodies ganglion for PNS nuclei for CNS This time when you have two connecting neurons you name them preganglionic communicates with CNS and postganglionic neuron interacts with effector o Sympathetic vs parasympathetic Sympathetic 0 Function is ght or ight Ganglion location is near the spinal cord Parasympathetic 0 Function is rest or regroup Ganglion location is located closer to the effector organ that is going to be impacted Both at our preganglionic require ACh to be released We also see ACh released in the postganglionic for the parasympathetic For the sympathetic in the postganglionic norepinephrine or epinephrine are released 0 Epinephrine and norepinephrine can be considered adrenaline 0 Question why do we need these ganglions in two separate locations rather than on top of each other We talked about the spinal cord and the fact that having the dorsal afferent and ventral efferent is better for an individual than having it reversed DAVE If we switched them we would still have a functional system If we took the ganglion and put them both in the same spot both in the middle rather than one closer to the CNS and one closer to the effector organ Why would the communication system be destroyed if they were both put in the same spot of the neuron The reason for this is to keep the messages distinct For example ACh is what s needed to deliver the messages and ACh is all the same but they each carry different messages If you put them both in the middle then the message might get screwed up Our sympathetic system has another way to work 0 Adrenal medulla It is a ganglion that releases to plasma We don t release neurotransmitters Messengers that move through the plasma are called endocrines Ganglion that releases to plasma endocrine gland Speci cally they release epinephrine and norepinephrine How do people know about big storms Sirens that alert everyone Distant organs 0 Usefulness of vestibular system visual tracking and the coordination and special recognition 0 Parasympathetic vs sympathetic respectively I Contract pupil vs dilate pupil Cardiac output down vs cardiac output up Contract bronchioles vs relax bronchioles 0 Why do we want out lungs to relax If we think about it when muscles are relaxes tubes are bigger thus allowing you to get more air in there Why don t we keep tubes big all the time Not just oxygen comes in when tubes are enlarged Risk of pathogens In ght or ight we shut off our digestive system Takes too long to get the energy from digestive system so it shuts down instead This is why athletes don t eat right before an event Once they are done digestive process continues Afferent sensory Nervous System 0 Registering stimuli and passing that information along to CNS Stimulus gt receptor gt afferent neurons O O O O 0 O O Stimuli include Pressure temperature light sound and chemical Sound is not exclusive Receptors include Afferent axon terminals or specialized cell They are speci c to the stimulus type pressure stimulus speci c to pressure alone They will produce receptor potentials from the stimuli They are really just graded potentials renames because they happen in receptor cells Afferent neurons Generate action potentials which is what moves along our afferent neuron They convey information to CNS regardless of how far from the CNS it is Sensory receptors two designs Directly by neuron end Option 1 Receptor cell to neuron end Option 2 Our nervous system s goal is to get a message from A to B as fast as possible First option happens faster which means we will see the second option more We are giving up speed so what s the bene t Having the second cell that slows it down allows us to make a lot of changes in how the cell is set up We can do specialized adjustments much more ef ciently Types of receptors Mechanoreceptors pressure or stretch Thermoreceptors temperature Photoreceptors light waves aka photons Chemoreceptors chemicals Nociceptors pick up painful stimuli heat or tissue damage When you get a paper cut activated this Somatosensory releases cytokines which attack bacteria and viruses They also attack pain receptors which is why you ache when you re sick Sensory Receptors Coding intensity location Sensory transduction When you poke your eye also causes a change in vision Example hand on a stove If we don t know where the stimuli are we could make the situation worse The stimulus itself is going to be variable How do we get something like pressure turned into an electrical message We need to take that pressure and get it to change our membrane potential By impacting the channels present we can change the membrane potential How many channels open depends on how we change the membrane potential We know that when we have these changes in our membrane potential that we change the graded potentials We want the size of our graded potential to match the stimulus Bigger stimulus will give you a bigger graded potential How do we turn them into action potential We need excitable cells Is our afferent neuron an excitable cell Yes they are capable of action potential Now we need to have our graded potential being created be a threshold potential There are going to be some signals where we register a stimulus but never send a message because they are subthreshold What makes neurons excitable Voltagegated sodium and potassium channels A bigger stimulus will trigger a bigger action potential Variable AP pattern not magnitude When we get to our interchange between afferent and interneuron we re not going to be able to stay as action potential There will be a synapse which interferes Neurotransmitters are released in this case When we have more action potentials hitting the end of that afferent where we have neurotransmitters ready to exocytosed more action potentials means more neurotransmitters ready to exocytose There is a variable neurotransmitter amount More neurotransmitters equal to a bigger stimulus When we have an increased stimulus we have an increased action potential frequency which results in an increased number of neurotransmitters First we have a receptive eld area covered This area means we re talking about afferent neurons We notice because it s missing dendrites and the cell body is out in the PNS not in the CNS which is exclusive to afferent neurons The axon terminal covers the receptive eld If we have a stimulus that just hits one spot of the receptive eld we re going to have it respond If it hits a bigger area of the receptive eld we re still going to see a response It doesn t matter how much of the receptive eld it hits we will still have the afferent neuron respond When we can localize where that is the receptive eld the brain will only know that it s somewhere within that speci c receptive eld If there is a big and small receptive eld next to each other the smaller receptive eld being hit is better to localize Size is related to localizing The smaller the better The ability to localize gets harder inverse with a bigger receptive eld I Another concept is that we can have different densities If we have a lot of small receptive elds in the area then we have a higher density We can also cover that same area with fewer larger receptive elds This gives us a problem in the area of sensitivity If we have two stimuli how likely are we to register both instead of combining them as one stimulus With sensitivity it s two But if sensitivity is reduced it gets combined to one Why is it that I can feel pressure more in my ngertips than in other areas of my body No because we have a higher density in our ngertips It s hard to have two different things on you ngertips and not be recognized as two different things as compared to the elbow which is less sensitive Another thing that is possible is that these receptor elds overlap We refer to that as getting recruitment For example you have three receptive elds next to each other Stimulus hits the middle one the most but the ones on the left and the right also gets hit The middle one has the greater intensity and the other two have less intensity A second way that this overlap helps us is that based on the idea of grade school with Venn diagrams We have areas of overlap in these receptive elds Overlap area helps us with localization because the left and right ones allow us to see which receptive eld the middle one is sending the strongest response to the stimulus 0 Lateral inhibition what happens when we bump into something Or when someone goes up and nudges you We rub that area and the pain goes away However when we stop rubbing the pain will sometimes come back We are using the concept of lateral inhibition Lateral inhibition is a way to improve localization by taking away part of the message It essentially sharpens the pattern contrast Out of three receptive elds the middle one gets hit but the brain thinks all three are getting hit We have crossing over happen to hyperpolarize We see a crossing over left has to cross over the middle s inhibition at the same time as the middle crosses over to hit the left one When all are inhibited what happens in terms of polarization and charge Left and right get dropped out and the brain knows to focus on the middle receptive eld Think of a painful stimulus as the middle one With mosquito bites you want to scratch around it oThe ascending pathway in CNS It goes through the brain stem then to the thalamus then to the cerebrum with cross For example left hand is linked to the right hemisphere Our cerebrum does things very particularly We have speci c brain regions visual auditory taste lnput can be impacted by output The brain can say quotEnough is enoughquot Most of the time the brain needs to do that You literally have hundreds of thousands of receptors sending information to the brain an overload and the brain needs to say enough Imagine being in a crowded room you need to tune out some people so you can focus Imagine walking around with a new pair of pants or wearing a new watch You eventually stop noticing the presence of that item on you Somatosensory System it is a more in depth version of the sense oftouch oThe information comes in from the skin and receptors associated with it But there is more to it It also gathers information from our muscles How contracted and warm are they From our bones how much pressure are they experiencing From our tendons and joints It is more than just quotwhat is touching usquot 0 Type free or modi ed afferent terminals If we are tweaking it we are only tweaking the end of the afferent neuron This is the faster of the two systems which one is the other one 0 Cars have a ton of warning systems They will have lights ashing sound etc About two years ago cars started coming out on the market and instead of a noise or light they made the steering wheel wiggle because it s activating our somatosensory system which is faster than our visual or auditory system In other cars the seats vibrate 0 Components Thermo and mechanoreceptors The latter are pressure receptors Nociceptors register pain What do we interpret as pain Detect products of damaged and immune cells Cytokines way immune cells communicate with one another might be used to register Think about a house there are certain things that you shouldn t see on the front yard like a toilet or couch sitting outside Some external factor caused those things to come outside Physiologically a cell may have been ruptured Nociceptors will pick up a cytokine connection and register it a pain only if it notices that something is off As far as that going to our brain it comes not just in a halfhazard brain but it comes as to where that information comes from It is spatially related positioned in the brain It is a cortical projection in terms of what gets activated and it is spatially input in a way that says that you ngers are all together rather than a nger being next to your toe Homunculus means quotlittle manquot We can change the size of that projection but only in a limited fashion Auditory System 0 Info sound waves Sounds are waves that are coming in and impacting us We can t see those waves but really it is like dropping the pebble into water Dropping a tiny pebble creates tiny waves compared to dropping a boulder o Stereocilia in terms of our categories those cells are our mechanoreceptors The mechanoreceptors are in the O O O O O O 0 O cochlea Also know as cochlear hair cells What do we need to know about the ears Basic pathways the sound waves travel Comes in through out ears Our voices sound different to ourselves because our voice comes in two ways rather than just in out ears External auditory canal canaltype structure that carries up to a structure that creates a block at the end of the canal known as the tympanic membrane or eardrum Inside the eardrum you have the middle ear air which is open to the throat area That s is why when you have a pressure difference you have a pain in your ears which causes you to pop you jaw That allows you to get some air in the middle ear Our cells are water dependent so we need to convert these airwaves of sound into water That is where the cochlea comes in Cochlea turns airwave into a water wave That is what the Stereocilia picks up The bigger the airwave the bigger the water wave proportional Once those changes are registered they go to the auditory nerve which then goes to the auditory part of the cerebrum What is it that we have in terms of coating so that our CNS can understand what is going on around us The cochlea encodes those waves We have sterocilia that has a receptor cell that then passes the information on to the afferent neurons The extra receptor cell picks up those messages What do they pick up The stereocilia little hairs actually bend as that wave pushed on them Mechanically gated potassium channels open as a result of the bending of the stereocilia which allows the potassium to enter which changes the polarization of the cell With enough bending you open voltagegated calcium channels that when they open will allow calcium to enter Based on synapse strength calcium will allow us to exocytose neurotransmitters The neurotransmitter gets picked up by afferent and goes to CNS What is it that we end up having coded in the cochlea Loudnessamplitude of the sound determines the amount of bending of the sterocilia Frequencypitch talking in high pitch or low pitch How many waves hit you at a certain time Waves hitting you fast are a higher pitch slower waves hitting you are lower pitchdeeper voice There are different stereocilia in different parts of the cochlea that bend to different pitchesfrequencies When we have high frequency short compact waves they will hit the beginningbase of the cochlea 0 When we have lower frequencies longer waves they will hit the apex of the end of the cochlea 0lf we had a biggerlonger cochlea we would be able to understand and pick up lower frequencies Babies respond better to higher pitch than lower pitch Which is why big muscular guys will talk in higher pitch than lower pitch The reason older people can t pick up on really high pitches is because with time the stereocilia in the base the earlier ones near the base get damaged If you want them to hear you drop down your voice In terms of hearing we need to know how loud it is know the frequency and even more important we need to know what direction the sounds are coming from the position of that sound so you know whether to go toward it or run away from it In terms of the cochlea the location of space and source of that sound cannot be determined However we have two different cochleae Whichever one gets hit rst is where you know where that sound is coming from Vestibular System 0 Gives information about the position of your head This is important because where your head goes your body follows This is a critical system in terms of being able to do balance and coordinated movements We base those things off of where our head it Once again we use stereocilia but this time they don t use the sound but rather they use waves created by the water sloshing around in the ears We have water sloshing around in SEMICIRCULAR CANALS We have three of them one for each plane As we move the water will move in these canals based on how our head is rotating Depending on which plane we are moving more in the particular semicircular canal will activate the stereocilia more 0 Utricle and Saccule they have otoliths in them which are rocks in our head We want those rocks in our heads because they serve as a reference point for gravity Utricle and Saccule gives us the acceleration relative to gravity Having gravity is very important shows it by knowing our position is a problem If you go into space or water the buoyancy will take away the reference of gravity The vestibular system won t know whether to go up or down Look for the bubbles in order to know 0 What is the usefulness of this system Movies before 80 s and before didn t have a lot of action components because when we move and walk our heads go down and up because of the way the body moves when it walks ls somebody holds a camera the camera goes down and up However if we watch the movie we wouldn t notice Cameras were created to take away that bounce Phones nowadays have that process where they keep things similar Visual tracking is important Helps us with coordination and spatial recognition Monday February 17 2014 Visual System 0 Energy waves that impact us They ones we register and see as visual stimuli are because we have receptors that respond to those levels of energy Most birds can see ultraviolet light because they have receptors that can pick up that range 0 How is it that we register these things Through PHOTORECEPTORS they register those photons energy receptors 0 Components of the eye Cornea and lens focus image 0 Hits the retina the cornea lens doesn t match up to the lens of the eye which then requires glasses Retina transforms photons into a signal Happens in the back of the eye The thing about the retina that s weird is that if we were taking an engineering class where we were designing a camera that could take pictures and catch photons we d fail if we set it up like an eyeball Photons have to go through afferent neurons in order to get to the photoreceptors An octopus has its receptors be the rst thing the light hits which means it can see in the dark 0 The afferent is in the front We pick up and start our signaling process by sending photons to the back then the signal moves forward to the afferent neurons to convert the signal so that it can go to the brain making a Uturn past the photoreceptors There are no receptors where the afferents exit The area where all the axons go out is considered the BLIND SPOT 0 The encoding process both pick up on photons Rods still stay active in lowlight conditions Picks up more blackwhite Cones loses effectiveness in lowlight conditions Work better under nice bright conditions Picks up more colors Which is why when we lose light we lose colors and therefore we lose the cones Color vision is based on three cone pigments BGR The red cone pigment responds differentially Yellow gets a little bit of activation from the green pigment no activation from the blue pigment and mostly red pigment achann 0 Basically tells the brain quothey we re picking up a little bit of activation from the green pigment and a lot of red let s classify that as yellowquot Cones and rods are the photoreceptors 0 Algorithm present in visual cortex is what gives us the spectrum that we see 0 Color blindness is an issue with the cones They are not missing cones or have fewer cones They are simply lacking pigments Instead of having receptors respond in three different ways RBG we have a shifting in terms of response Basically the curve that picks up green pigment may be lined up with the red curve which causes redgreen color blindness happens to 1020 white males This creates an issue with streetlights so they added a re ector around the entire perimeter so that colorblind people don t have to guess which light is on Chemosensory System chemicals must be dissolved to be picked up by this system 0 Chemoreceptors 0 Components External to detect changes in outside environment we have TASTE and SMELL This helps us locate food sources and avoid nasty foods Internal pH cellular metabolism and 02 we know from equation 3 that we can get a pH problem if we don t know out C02 Cl39 etc 0 Taste receptors are in mouth and throat What is an aftertaste That s the food accessing the receptors in the back of the throat When people taste wine they gargle it so that they can also taste the aftertaste Surface area and quantity of receptors are direct More surface area more receptors What kinds of receptors do we have in terms of taste 0 Salt Na channels You re making more sodium on the outside of the membrane Sour the amount of H there Determines pH because sour is an acid component The H messes up movementblocks Kchannels Sweet sugars bind Bitter various substances bind There are subcategories of bitter We avoid things that are bitter High levels of bitter contents are toxic Umami glutamateMSG agonist binds Umami means quotsavoryenjoyable avorquot You will eat more things with glutamate Make two brownies and add MSG to one People will prefer the one with MSG glutamate is a key component for cell metabolism pathway Glutamate is important for the Krebs cycle If we needed more glutamate we want to eat more Umami Likely adding a fat receptor soon People have a receptor that adds fat Sense of smell 0 Olfaction in nasal passages Scent that we re picking up comes in airborne lt detects dissolved chemicals When nose gets really dry you don t smell things as well 0 Receptors Differ in type and in quantity We don t all smell the exact same things if we were in the same room We gather same lightauditory information but not the same olfactory information because of different types and quantity These receptors only last about two months What we were focusing on smelling 2 months ago can change Working in a job that has a distinct smell for a while makes you unable to smell that eventually If a smell is constantly in the environment you won t smell it in 2 months Perception 0 We can change what we gather Even what we gather we have to process and turn it into something else That s what perception is about It s about how our brain interprets these signals All of it happens in our cerebral cortex Most of the time we combine different signals When talking about taste we re talking about just what happens in our mouth But for example if we have a stuffed up mouth our perception of taste changes That is because that taste is what s happening in our mouth but we smell it at the same time If either changes the whole overall taste changes If you eat potato chips and we plug up our ears it might taste different because you don t have that crunchy sound When you see a speci c thing ie potato chips you expect a certain taste from a certain sound the crunch ln autistic people they process auditory and visual but not at the same time Visual goes at a normal pace but they don t process anything auditory at the same pace Kind of like watching a movie where the lips moving and the sound don t match up This confuses them and then they either try to avoid looking in order to listen or vice versa We are better at doing detections that we re consciously aware When guys look up and talk to a female do we know when a girl is at a point in her cycle when she can easily get pregnant or not Girls have genes that can see how a guy s genes match up with hers to make cute kids Perfume aftershave etc prevent girls from smelling that Somatic Nervous system skeletal and muscle 0 Skeletal striated Attaches our bones to our bones and allows our bones to move via tendons Ligaments are bone to bone Tendons are muscle to bone Skeletal muscle supports and moves skeleton It s mainly voluntary control Cardiac muscle also striated The one place where we see this muscle is in the heart It is not voluntary This is autonomic and involuntary control Smooth muscle when we look at it there are no striations We nd it in sheets around the organs to make organs bigger or smaller Contraction alters the ow GI tract more blood moving to particular area more things we eat move through digestive tract more air into our lungs EXTRA CREDIT 2 BLUE 2 GREEN 3 BLACK AND RED SQUIGGLY Skeletal Muscle O 0 Muscle gt Organ Myo bers Muscle cell ber Multinucleated Myo brils Bundles Myo laments Basic structures 0 Think myosin 0 Thin actin Myo laments make up myo brils and myo brils make up myo bers Sarcoplasmic Reticulum SR Plasma membrane covers myo brils and each myo bril is surrounded by Sarcoplasmic reticulum We have SR because it s a holding site for all calcium in our muscle cells Cells typically are low in calcium Basic intracellular uid is low on calcium Transverse tubules 39lT Transverse going across When we look at muscle ber we have transverse tubules If we bring plasma membrane down into the cell that means we have interstitial uid inside the TI39 These channels allow interstitial uid to gain access to the inside of muscle ber which is critical in the function of muscle bers Once calcium binds to Troponin causing the Tropomyosin to move which When contracting it pulls closer to the M line Calcium is going into the Myo lament which is inside the myo bril In a muscle ber you also have mitochondria This is a key for making ATP in aerobic conditions Anatomy of a Myo lament Zline disc thin connections A 3dimensional disc that goes across the Myo lament Our 2 line is where we see a connection between our thins Keeps them in place O O O Sarcomere functional unit 2 to z A in size How do we get it to be small or how do we get 2 lines to come closer together I band only thin Striation comes from light and dark banding patterns The light bands are the lbands that are seen When we look under a microscope we can visibly see the lband If we look at a muscle we know difference between contracted or relaxed When it s contracted light areas go away When relaxed light and dark are about the same A band length of thick To shorten Sarcomere there will be no change in Aband but a shortening in l band Proteins of A bands cannot change in size M line midpoint between two z s We can see an area where there is only thick H zone only thick It will change in size More anatomy of muscle function 0 O O O Actin thin lament Each one of these individuals is a protein called actin but the structure basically creates an appearance of a double helix shape It s almost a rounded structure like a pearl necklace that you start twisting Each actin has a myosinbinding site which is where the two proteins interact Tropomyosin structure associated with actin Bound to actin and one of two proteins In the relaxed position it covers over the myosinbinding site It s not binding at that site but it s blocking it like the sodium inactivator Troponin bound to Tropomyosin and actin There s a crescent shape near the top That is the binding site that allows calcium to interact with this protein The only protein in the myo ber that binds to calcium Myosin thick lament kind of looks likes a golf club It has a binding site on the tip where it nds actin It is also the only one that has a binding site for ATP Crossbridge exible Creates a bridge across from thick to thin Across the two Myo laments At rest Tropomyosin blocks actinmyosin binding If we bind something to a protein we will have a shape change Innervation of muscle 0 O O Somatic efferent and peripheral Myo bers muscle bers Different muscle bers are connected to a motor neuron The motor neuron creates the effector that causes the O O movement Motor neurons are somatic efferents Axon endings wi branch off to different muscle bers One neuron can innervate several myo bers Motor unit what works in a group A motor unit is composed of ONE NEURON AND ITS GROUP OF MYOFIBERS Function of a junction 0 O O 0 Inside of the myelin Schwann cell because of PNS you have graded potential Then you have action potential which causes a change in membrane potential Membrane bound receptor acts as an ion channel which is ligand gated The opening aows sodium to enter the cell We just changed the membrane potential via depolarization less negative which makes the cell excitable and then you have voltagegated channels with inactivator ready It can become the threshold potential which then turns into action potential We took electrical message passed it along via ACh and got it back as a chemical message First trait about ACh is that each and every time we use them we need to clean them up so that the message stays distinct How do we get rid of ACh AChesterase We want ACh to get there so that we get muscle contraction Contraction Action potential conducted along plasma membrane into Tl39s Action potential opens up voltagegated channels that allow sodium to in ux into the cell In SR voltagegated calcium channels open Calcium gets released and moves around in the cell and is able to bind to the binding site on Troponin When this binding occurs you get a shape change That shape change changes the Troponin and it moves away from its blocking position to that site and exposes myosinactin binding site Now we have that our myosin ADP and Pi is able to bind with our actin Crossbridge Cycling a series of conformation changes FIGURE 915 Myosin ADP and Pi binds actin We just bound a protein to a protein so the shape will change The shape change will be to our head of our myosin It will change the shape of the binding sites where ADP and Pi are attached if we change shapes of binding sites we alter the affinity degree of binding change the shape or charge makes it less able to hold on to that ADP and Pi so they come off We are releasing a phosphate which not only gets a shape change but we get a release of energy since it s a critical energy component 0 This causes Crossbridge to ex We bind an ATP to the myosin because it s a thing that is bound to our protein myosin which changes its ability to hold on to myosin which then releases the actin We need to reach out again we used energy from phosphate to pull how will we energy that big move of our Crossbridge ATP We break it down do equation one and use energy to de ex cock it in order to put it back into position so that it s ready to grab calcium that is still present so that we can start the cycle over again How much do we get out of each pu from the Crossbridge cycle About 10 micrometers Actin moves relative to myosin Rigor mortis no exibility When you die you don t make any more ATP We need ATP to do the release when it doesn t do that then the myosin stays together with actin and you have essentially created the equivalent of Velcro with your muscles 0 The levels of ATP drop depending on what the individual was doing before temperature etc That gives them an idea on how quickly the ATP should ve decreased which can then tell them how long the person has been dead Our ZIines move in as our heads keep ratcheting in our actin and moving it closer to the MIine which is bringing our two ZIines together which is shortening our Sarcomere Filaments do not change in size themselves Aband does not change in length because it is the length of the myosin which doesn t change in size lband however does get smaller The light band band starts to disappear but the Aband dark stays the same Hzone is the opening in the middle of the Aband that also doses up a bit More overlap means that lband and Hzone get smaller but Aband stays the same lband and Aband NEVER overlap they will always be next to each other 0 Relaxation We want to put calcium away at the end Where do we get calcium The Sarcoplasmic reticulum so we need to put it back in the SR but to do so we will create a gradient We have to use an ATPase pump We need ATP to relax our muscles Once the calcium is put away it s no longer there to bind to the Troponin The Tropomyosin then blocks the myosin binding site and there is no Crossbridge cycling In terms of that unless we release more calcium which would require depolarization and action potential of the Ttubules Our muscles contract when we touch something electric because instead of our brain sending the message we put electrical signal directly to our myo bers which causes them to contract The idea of muscle contracting as a result of action potential moving on our skeletal muscle ber takes about 12 milliseconds That s still really fast There s still a delay before we have a contraction This delay is called a latent period something starts and actually seeing something Why is it that we have this latent period It s about calcium being able to increase in the cell become available get to places where it s supposed to do its job and actually do its job We know it s doing its job when we see the muscle contracting ln shorter terms it is an increase of calcium in the cell The trigger is 12 milliseconds but the contraction can last up to 100 milliseconds Getting the calcium out of the cell is what takes 100 milliseconds Imagine increasing the calcium as just dumping clothes on the ground and decrease in calcium as putting clothes away individually Muscles need a lot of ATP Dissociation of myosin from actin We also need the same ATP to do our equation one release its energy so we can create de ex and be ready for the next pull Every 10 micrometers of movement requires one ATP 0 We also need an ATP for every calcium we put away for relaxation Muscle Making ATP 0 Two ways to make ATP Substrate level and oxidative Phosphorilation Substrate level includes glycolysis and Krebs cycle and also Creatine phosphate 0 We have a phosphate that we move over to our ADP to make our ATP via equation one 1 creatine phosphate makes 1 ATP Creatine phosphate is a nice source of ATP because it takes just ONE step to get your ATP Glycolysis is a tenstep process the quicker the better Only drawback is that one creatine phosphate gets us just one ATP which moves us just 10 micrometers The creatine phosphate is going to get used up very quickly When you use a muscle creatine phosphate is the primary source but it runs out pretty quickly 0 Packing in creatine phosphate changes the Osmolarity When we raise the number of things in a cell the interstitial uid stays the same and Osmolarity inside the cell increases it will go toward the higher Osmolarity so the cells are going to get loaded up with water 0 Another problem with creatine phosphate is that it is not a nice compound Can create toxicity issues lnitial source limited supply don t get more than limited supply but once you re done with the activity turn that creatine phosphate into ATP Glycogen is the reason that when athletes carb load the night before an endurance event they do it in order to store more glycogen Glycolysis makes ATP creatine has 11 ATP ratio and Krebs cycle makes 2 ATP When do we rely on glycolysis in terms of creating ATP When we do intense exercise put you in anaerobic conditions which we know that out of our components glycolysis is the only one that can run in those conditions It still happens when you re doing things aerobically If we re working off of it anaerobic we re also making lactic acid When we rest we need to clear away that lactic acid Like our creatine phosphate we can replenish components and eliminate lactic acid and we can do glycolysis again whether aerobic or anaerobic Third source of ATP is oxidative phosphorylation Creatine makes one glycolysis makes 2 and oxidative phosphorylation makes 3234 However we have to stay aerobic not overuse your oxygen supply which means we can only do moderate exercise Once again Krebs cycle makes 2 ATP just like glycolysis Krebs cycle isn t included in the gure because it would confuse us too much In terms of activity level the Krebs cycle happens AEROBICALLY ONLY because it relies on that recycling from oxidative phosphorylation Whole muscles 0 Contraction produced by Crossbridge cycling Many sarcomeres getting shortened at the same time More contraction needed more sarcomeres will be shortened Think of example of pulling a rope and who pulls harder When you are using your muscles you will always have an opposing load Generating a force tension If you have a 10 kg ball in your hand you need to create enough tension to oppose the 10 kg weight of the ball For basic physiology you would use more than 10 kg to oppose the 10 kg ball in your hand it s more than 10 kg because you have your hand forearm and all of the bones and muscles involved In exercise physiology they would say the tension generated would be exactly 10 kg because we focus on everything involved We only get our muscles to shorten when we create enough tension to move that load We know that we can work our muscles without having shortening occurs Contraction does NOT equal shortening Isometric contraction iso same and metric length we have no A in length We have a whole set of exercise components involved with isometric contractions Examples include pushing and pulling loads too big to contract If the tension is less than the load you will not have shortening happen hence the no change imagine her picking up the podium lsotonic contraction no A in tension We will have our tension greater than our load therefore we will see shortening occur Why doesn t the tension keep building Because bigger tension means more Crossbridge cycling which means more ATP spent Eccentric contraction muscle is actually lengthening In this situation the muscle has to deal with load This happens because the load is greater than the tension For 0 getting out body to move around we focus more on isotonic contractions sotonic contraction continued how much we do in terms of that contraction A bigger shortening means we ve done more contraction When our tension is greater than our load we need a moment of isotonic You have an initial period of isometric contraction tension lt load Imagine bodybuilders trying to deadlift they have to build up the tension before they can actually lift up the weight The shortening of the muscle only begins when the tension is greater than the load As we go from small to medium to large load bigger load the longer you will spend in the isometric region before you actually contract However the bigger the load the lower the velocity How fast can you achieve that process The last thing is response The bigger the load the smaller the response Think of doing a bicep curl A full response is that the hand should go all the way up to your shoulder The smaller the weight the easier it will be to get it to your shoulder If the dumbbell is bigger your ATP will run out as you are in mid curl What is the impact of repeated stimulations The impact of repeated stimulations will give you a summation of what kind of tension you can generate In respect to neuron communication building off hyperpolarization is like building off tension Keeping tension above zero or maintaining a contraction is referred to as tetanus The bad tetanus is referred to as unfused There is partial relaxation between stimuli Fused tetanus means hitting the muscle so frequently that there is no opportunity for voltage gates calcium channels in SR to work You have maximum contraction happening Not all muscles are created equal Different muscles in our body are focused on being better at certain things There are differences in our myo bers that make up our whole muscles Speed of contraction fast vs slow What is variable in terms of contraction speed The variable part comes down to Crossbridge cycling Almost everything about our cycle is about conformation changes binding and unbinding The only exception is breakdown of ATP which relies of ATPase Some of these enzymes can do the job quickly others take a longer time to break down the ATP It s about that hydrolyzing of ATP The speed of contraction differs with respect to amount of ATPase activity Hydrolyzing ATP on Crossbridge The faster contraction uses ATP more quickly We can get more tension out of it because every time you run the cycle you get a pull How do the myo bers make ATP Mechanism for making ATP o In terms of the muscle we think about aerobic or anaerobic because that ties to how the muscle makes ATP We could have muscles that try to stay oxidative maintain proper oxygen levels or muscles that will for sure run out of oxygen so they try to do things anaerobically glycolytic Oxidative key is to make sure we have enough oxygen available We will see a lot of blood vessels vascularity The polarity of oxygen is nonpoar and it is small so it means that it can cross the plasma membrane with no problem If we want myo bers to stay oxidative we want to load up the inside of them with oxygen But the gradient will cause the oxygen to go right out Solution to that is to trick the gradient to stay inside the cell by packing the outside Another way we can do it is by capturing the oxygen on the inside of the cell and not let it go outside by binding it to an amphipathic and thick protein That protein is called myoglobin Glycolytic there are very few mitochondria here It takes energy to build mitochondria but if you won t use them why build them If we do gycoysis alone we will get 2 ATP from one glucose in gycoysis Those 2 ATP will move us 20 micrometers from Crossbridge cycle We need a bunch of gucoses But you can t have too many individual glucose particles because of Osmolarity this is why you need them chained together in order to prevent a big hypertonic solution inside the cell 0 Three types of bers dark medium light Slow oxidative enzyme low ATPase activity that does crossbridge cycing but has to wait for enzyme to do its job combines with having the muscle get its energy oxidatively This type of ber is very slow which means that it uses up ATP very slowly and maintains constant tension for an extended period of time Oxidative makes a lot of ATP so it can last a ton Imagine someone making a six gure income but living at poverty level The question is how much ATP are you making and how quickly are you using it Make a lot Use it slowly Fatigue means running out of ATP Fast oxidative glycolytic high ATPase To be oxidative you have to run through glycolysis rst keyword is oxidative We run crossbridge cycling faster which means more tension However we lose a lot of tension here Inputs remain the same but our outputs have gone up because we run through crossbridge cycling at a much faster rate Fast glycolytic high ATPase high glycolytic We are able to get the most amount of tension created but it is not sustainable at all The tension decreases very fast Very quickly fatigued In terms of muscle tone they will be a combination of all three types When we see muscles that are redder the more myoglobin you have the more red it will look Oxidative red Glycolytic white In birds that do more ight they have much less white meat than dark meat For example chicken breast is white meat but thighs are dark meat because they use their thighs to walk 0 Genetic basis We know that there are differences within humans Some people are better built for longdistance and others are better shortdistance This is due to a difference in genetic setup Proportion can be modi ed You can improve your muscles to make them more oxidative or gycoytic depending on if you want to train for a marathon or for a 100 M dash 0 Impact of usedisuse Change in muscle structure andor function Is it focusing more on being an oxidative or gycoytic muscle Disuse atrophy disease broken bones couch potatoes Use hypertrophy exercise Aerobic oxidative To stay oxidative as you do aerobic exercises you want to make sure the muscles have the right oxygen levels so aerobic workouts will cause an INCREASE in vascularization Also inside the muscles being used you will notice an INCREASE in the number of mitochondria present in those muscles You also DECREASE the amount of fatigue 0 Anaerobic quick activities like sprints You will run out of ATP quickly but the objective here is to get the biggest tension possible You need an INCREASE in myo ber diameter You also get an INCREASE in glycolytic enzymes If you aren t using your muscles why spend ATP on building them and making them bigger You need energy in order to maintain all those proteins You don t use them the body assumes you don t need them and the body will shrink the muscle in order to preserve energy Controlling body movement Motor commands originate in motor cortex When we talk about skeletal muscles we can always stimulate them To be able to move joints in two directions you need to have two pairs For example biceps and triceps O O O This group or muscles are known as the exor and extensor Proprioception a sensory system It gives information about the load on a particular muscle which leads to the position of our body You have stretch receptors 0 Muscle spindle vs golgi tendon organ We can see how much pressure is happening on the tendon and muscle ber which the brain then processes with an algorithm Afferent signal goes to the brain and you have local re ex circuits Feedback then goes to the brain and tells it quotwe are at the desired positionquot Eccentric contractions that are sometimes not caused by you but because of a load bigger than you can handle We have re exes to protect ourjoints As opposed to re ex arc we use it in a very speci c manner Spinal re ex you have an involuntary contraction We got to get those local re exes tell us that we have a dangerous stimulus and we will then get a quick turnaround to impact proper neurons so that we alleviate that danger How It depends on how we impact the joint 0 Example is the kneejerk response The rst step is hitting the patellar ligament We are going to send that positive input to our spinal cord It will still go to our cerebral area but our spinal cord realizes that you need something faster than to wait for the brain to tell you what to do In terms of what happens in the spinal cord the positive input will go to the extensors which make the joint bigger However this means that you will have a negative input to the exor Can we really inhibit our exor In this case our exor is skeletal somatic so no you can t How do we accomplish this We say that we are impacting the muscle but what really controls the muscle we impact The motor neuron If we get it to not talk to the exor any more the exor will stop pulling In which case the extensor will have its way Withdrawal response you grab for a glass You realize you move your hand back and then you realize it s hot With the feet say you step on a tack you get painful stimuli in the foot so you stimulate the nociceptors regular somatosensory system If we pull away from where the pain was occurring hopefully you can limit the damage This means you stimulate the exors and inhibit the extensors If you stimulate the extensors and inhibit the exors you are driving your foot further into the tack Not just that but you shift your weight which means that you have to extend the other leg so that it can support the shift in weight In other words you stimulate contralateral other leg extensors and inhibit the contralateral exors This results in a coordinated movement of the entire body away from the painful stimulus Smooth muscle 0 Where do we see it in terms of location Lining things such as organs Smooth muscle is under autonomic control so you don t have to worry about digesting your food or worry about your blood pressure urogenital ducts to urinate and have some fun and impacting the release of some gland components 0 Characteristics Not striated and it s layered Under autonomic control and With skeletal it was all about myosin and actin interacting Here it s about Myo lament arrangement The difference between thick and thins here is that there is no Zline present in smooth muscle You have what are called dense bodies instead Zlines connected and created a parallel arrangement between thick and thin in skeletal muscle With smooth muscle rather than have a linear pull everything pulled in one direction you have a radial pull Imagine a ball pulling a bunch of things being pulled toward it at the same time There is still a thinthick pattern but you don t create lbands and you don t see Abands This is why you don t see striations Unlike skeletal where you have one Myo lament running the whole distance you need several cells to communicate in smooth If they aren t all synchronized and connected quickest communication happening by gap junctions your bladder won t have one giant squeeze You want one squeeze of you bladder with everything contracting at the same time This requires the gap junctions How do we get contraction to happen in terms of smooth 0 The starting point is by getting calcium into cytosol of the cell So an increase of calcium in the intracellular ln skeletal SR held that Might not be just autonomic but also endocrines or chemicals that come and bind and gets us to change It might also be about stretch bladder example There are some smooth muscles that contract at a regular schedule due to PACEMAKER CELLS You get the calcium in but there is no Troponin You also have Tropomyosin but it s not blocking You have calmodulin instead Its job is to activate and enzyme called quotmyosin light chain kinasequot Remember kinase does equation one meaning it adds a phosphate and phosphorylates myosin This causes a crossbridge to form and crossbridge cycling happens same as skeletal muscle Relaxation Myosin light chain phosphatase increases Monday March 3 2014 Endocrine System 0 The other communication system Bloodcarried signals Widespread effects Regulated by feedback mechanisms Speed Endocrine ltlt Neural o Pathway gland gt endocrinehormone gt effector Endocrinehormone o Differ in Type Mechanism of action what action may get to happen in the body 0 Types of endocrines Amine endocrines Derived from tyrosine C ring T3 and T4 Thyroid gland are nonpolar unlike the other endocrines Nonpolar endocrines can be an issue because they are in a polar environment Norepinephrine and epinephrine Adrenal medulla Dopamine is part of the hypothalamus Peptide Endocrines Synthesized as prohormone Prohormone pro means that endocrine is in inactive form means that it s inactive Helps protect component by being inactive To get ready to release it you need to exocytose them Meaning we need to put them into a vesicle and since when they re in this vesicle they re already isolated from the rest of the cell so once in the vesicle you turn them active In the vesicle they get processed into the actual active endocrine and lose the pro pre x We want to release them WHEN WE NEED THEM They wait for a signal IN THE VESICLE Similar to neuromuscular junction where the ACh waits in the vesicles 0 They are released on demand Examples include insulin hypothalamic releasing hormones pituitary endocrines and gastrointestinal endocrines Steroid endocrines Synthesized from cholesterol 0 Because of all those rings and we know we ve talked about cholesterol being amphipathic the steroid endocrines are lipophilic 0 Needs binding protein in order to move around the plasma When we activate an intracellular receptor we alter the DNA We either get more activity or less activity when working with DNA transcription Produced by gonads adrenal cortex and placenta Cholesterol shouldn t be completely avoided if you want properly functioning sex organs As far as adrenal cortex has a couple of steroid endocrines associated with it and also the placenta can produce and release some 0 Production requires steroidogenic enzymes Instead of going after the particular endocrine you go after the enzyme making the endocrine For example when you don t want a certain amount of testosterone to be present they can take a pill or do an application that doesn t go after the testosterone but goes after the enzyme that makes it o Mechanisms of action how endocrines work They are simply ligands that bind to receptors Hydrophilic bound to membranebound receptors Not usually a one step process they need to activate a second messenger system Hydrophobic can go right through the membrane and can impact DNA transcription How can we disrupt that ligandreceptor communication 0 We can go after the ligand but when your endocrine is the ligand you can do endocrine synthesisrelease For example with peptide endocrines being released on demand we can go after that Up or down regulate it 0 We can go after receptors We can take them away by hiding them or doing full catabolism We can alter its likelihood of getting to that nal destination or how long it s available This is called ALTER CLEARING We can put an agent out there that actually destroys the endocrine as it s moving through the blood 0 Doctors want a urine sample because one of the things that s in that urine are endocrines that are leaving your body In some instances is to get rid of them and in other instances it s about communication 0 Regulation of secretion Based on the concentration of substances in the plasma We talk about chemosensory system a lot because also the endocrine system makes sure that different levels are in homeostasis For example ions and sodium and potassium Nutrients glucose insulin sugar put away for later use Neurotransmitters ACh stimulates the adrenal medulla We also know about the interchange between nervous and endocrine system via hypothalamus and how the hypothalamic neurons receive input from other neurons The endocrines that release further endocrines can be tricky We typically won t have just one endocrine and then get the response With these other endocrines like the pituitary gland which stimulates other glands Endocrine system 0 Hypothalamus conversion factor from nervous to endocrine system Surrounds the third ventricle out of four in the brain Hypothalamus contains neurons that release endocdnes The pituitary gland is referred to as the master gland but the hypothalamus is the real master gland because it controls what the pituitary gland does There are two ways that the hypothalamus talks to the pituitary gland Hypophysis Infundibulum what is it Two parts to the pituitary gland Anterior Adenohypophysis portal vasculature 0 Seven endocrines that get released by hypothalamus and come and get picked up by anterior pituitary lt s known as hypophysiotropic endocrines Posterior neurohypophysis it s different because instead of releasing into portal vasculature the posterior is the location of hypothalamic neurons There are two endocrines that are released in this way Communication overview Stress provides neural input that says the temperature might be a little bit off and it needs to be adjusted Let s use the endocrine system to do that It tells the hypothalamus that there is a problem so it will release an endocrine endocrine 1 that binds to receptors on the pituitary gland anterior The response to that is to release another endocrine endocrine 2 which impacts a gland that releases a THIRD endocrine which goes to the effector target organcells Endocrine 3 goes back to both endocrines 2 and 1 Prevents you from overshooting Bene ts 0 Many opportunities to regulate andor 0 Ampli cation When we want to have more of a particular endocrine made we need more production space If we can get outside the brain area can t do it with the pituitary gland Ampli cation idea goes back to cell signaling section where we have one ligand be able to get us hundreds of thousands of responses One endocrine 1 can get you lots of endocrine 3 responses Thyroid gland will be associated with throat area it s okay if it gets bigger Adrenal glands can get bigger because there s space there that allows it 0 Our job now is to not see these sets of 3 as lines on a table but what are these endocdnes o Endocrine 1 comes from the hypothalamus There are 7 hypophysiotropic endocrines Five of the 7 stimulate the pituitary gland which causes an endocrine to be released We NEED TO KNOW THE SEVEN o Corticotropinreleasing hormone CRH cortico sounds like cortex Released by hypothalamus causes anterior pituitary gland to release adrenocortictropic hormone ACTH o Endocrine 1 comes from hypothalamus and it causes endocrine 2 to be released from pituitary o Thyrotropinreleasing hormone TRH goes to the thyroidstimulating hormone TSH 0 Growth hormonereleasing hormone GHRH gives rise to growth hormones GH released 0 Gonadotropinreleasing hormone GnRH causes TWO endocrine 2 to be released One is luteinizing hormone LH and folliclestimulating hormone FSH o Prolactinreleasing hormone PRF is a recent nd and addition lt impacts anterior pituitary gland to release Prolactin Lactin lactate mammary gland o The remaining two don t stimulate but rather inhibit o Somatostatin SS decreases the amount of growth hormone o Dopamine DA goes to anterior pituitary gland and counteracts to decrease the amount of Prolactin that gets released 0 Transmission pattern How does endocrine 1 actually get to anterior pituitary gland Vasculature It goes to the anterior via portal veins 0 Anterior pituitary hormones o ACTH gt adrenal cortex From there what s out endocrine 3 Cortisol ACTH is endocrine 2 adrenal cortex is the gland and Cortisol is endocrine 3 TSH gt thyroid gt T3 and T4 0 Growth Hormone GH gt liver responds to GH and releases endocrine 3 plus gt lGFl Insulinlike growth factor1 Growth hormone stimulates many other organs and tissues One of the big components of this is protein synthesis You need to make more proteins which means you have to break down other things In order to fuel this protein synthesis you will break down sugar storage and fat storage carbohydrate and lipid metabolism in other words 0 Another endocrine 2 is FSH and LH which impacts the gonads and the gonads will get us our sex hormones testosterone for guys and estrogen 0 We also have Prolactin which goes and impacts the mammary glands and doing so to increase the size of the mammary glands increases the production of mammary glands to yield in an increase of breast tissue and milk 0 We don t know the endocrine 1 for beta lipotropin and betaendorphin We don t know what they do but we care about them because we know that in other mammals and the likelihood is that they used to do the same for us when we were cavemen Betalipotropin allows for an amount of fat to quickly be added to the body Puts fats into circulation o Betaendorphin is a natural painkiller Extreme sympathetic situations will allow this to kick in Animals that are badly damaged seem oblivious to the pain because this has kicked in Posterior Pituitary Hormones Oxytocin causes lactation and labor contractions It also circulates in guys 0 Vasopressin impacts the size of blood vessels and also kidneys which comes to another area where physiologists are looking at isolated parts of our bodies Not only does it impact the size of blood vessels but it also impacts how much water our kidneys hold Antidiuretic hormone ADH is the name given by nephrologists Both of these also act as neurotransmitters in other parts of the brain Transmission Through the extension of hypothalamus These tubes do not follow the classic 3endocrine setup Why are the hypothalamus and the posterior pituitary considered one Thyroid gland has two lobes straddling trachea below the larynx In terms of composition we have a very key concept to get across This gland is composed of follicles Think of it like a supercell It is a celltype structure with a protected inside space and a boundary that limits access What we end up seeing with this is that the boundary are edged with follicular cells and their connections make sure to limit access in and out of the cell It is lled with colloid which is extracellular uid It s a protected space of intracellular uid It is hard to see in adults but it s really easy to see in a fetus because the thyroid is important for brain development 0 T4 AKA thyroxine and T3 Triiodothyronine We would see more T4 in our circulation T3 is the more active form The affinity is dependent on shape and charge T3 has the capacity to turn T4 into T3 The 4 in T4 are there because of 4 iodines If it loses one of its iodines it becomes T3 0 How do we get T3 and T4 put into the system Follicular cells have receptors for TSH Thyroid stimulating hormones cause stimulation of T3 and T4 That production happens in the colloid which is outside of the cell rather than inside of the cell and releasing it TH then inhibits TSH and TRH 0 Third job is to go out to the nuclear receptors which are nonpolar Most cells in our body can be impacted by these Exam 6 Review 22614 0 O 0 Explain the motor commands Exam 6 number 23 why does it matter if voltage gated opens only in the myo bers Neuron and myo ber makes up neuro T tubule SR surrounds myo brils and IT goes around the SR voltage signal comes into the middle of the myo ber Calcium oods inside the myo ber and binds to Troponin Once that happens we get crossbridge cycling Remember action potential goes along the membrane and TI39 allows interstitial uid to go inside the myo ber Basically a bunch of depolarization events down the membrane Picture an axon You have voltagegated channels opening up as you go down the IT You have voltagegated calcium cells in the SR that open up and cause a ood of calcium Troponin is bound to Tropomyosin Tropomyosin is bound to the actin This is located inside the myo brils which make up the myo ber The unit of TroponinTropomyosin makes up the actin ADP and Pi is bound to the myosin head It is in the relaxed position and the phosphorus and ADP causes it to ex only 10 micrometers After one pull ATP binds to it but it can t hold on so it lets go Relaxation Starting from crossbridge cycle it is still bound to the actin ATP needs to bind which causes it to let go You need to phosphorylate to de ex ATP is hydrolyzed split into ADP and phosphorus and it s relaxed again Look up the crossbridge cycle on YouTube Imagine that the Tropomyosin is the coil Exam 6 number 27 Which is a correct statement about TI39 39l39l39 are made out of the myo ber A is true 0 B is false because myo ber is the cell itself they take AP to the MYOFIBRILS o C is false 39l39l39 runs perpendicular 0 Exam 6 number 17 Striations are easiest to see when the muscle is relaxed because there s overlap of dark When the cell s relaxed When the muscle cell is contracted the lband and Hzone will shrink which will cause less visibility of striations The Aband is the entire thick and the Hzone is a subset of it 0 When light enters it goes through the rods and cones The light goes to rods and cones gets transferred to electrical signal Each rod has a neuron and each cone has a neuron The rods are bigger and work for night vision We need something bigger to pick up signals in lowlight conditions 0 Function of a Junction Calcium is always voltagegated Depolarization causes an opening to voltagegated calcium cells Exam 5 Review 21814 0 Exam 5 number 7 Efferent and inhibiting Example of wearing a watch You have an input that s continuously happening but after a while you want to block it out because either way you have thousands of inputs coming in at once It becomes slowly diminished over time Afferent doesn t inhibit cells only efferent does If you block the afferent that means you feel it o Breakdown of nervous system We have PNS and CNS PNS is divided into afferent sensory and efferent outputmotor Afferent is then broken down to somatosensory detects stuff in other parts of the body like what kind of stimuli like Nociceptors mechano thermo and receptive Receptive includes nociceptor mechano thermo chemo and photo Efferent pathway is divided into somatic you have control over this one skeletal muscle and autonomic controls cardiac and smooth Efferent is divided by sympathetic and parasympathetic Sympathetic moves away from set point parasympathetic moves it back to set point This is why autonomic is a two neuron system Whichever neuron is being stimulated more is the one that will send the messages to put the body in either sympa or parasympa You need two neurons because it will either excite or inhibit With somatic you only need one neuron because it will only excite Somatic is just a faster system You either have a faster system or you don t 0 Cerebral cortex is the place where two sound signals get registered and then the brain does the geometry to gure out where the sound came from o Semicircular canals they have water in them but the main function is to convert airwaves to water waves Helps with balance and knowing where you are You need both semicircular canals and otoliths to gure out where your body is positioned in space 0 Stereocilia are also in semicircular canals You will only nd stereocilia where there is uid otoliths semicircular canals Lateral inhibition a neuron will inhibit a neighboring neuron If a stimulus is stronger it is the FREQUENCY that is increased with it not the amplitude Axons hyperpolarize neighboring axons Recruitment goes down to the density and the sensitivity If you have really large receptor elds it will send a signal to the brain Doesn t matter how many points hit the space the brain will see it one point However if you have two receptor elds and one point each is hit your brain will interpret it as two signals Overlap between two neurons the brain knows what to register based on whether it hits just one or both neurons Intensity simply has to do with how hard it hits the stimulus Tympanic membrane is connected to three bones Stereocilia are voltagegated Intensity of sound wave determines how much mechanically gated potassium channels bend Explain the process of determining how loud something is again Pitch determines which stereocilia are being bent Middle ear is bones that take vibrations from the air 23 A is false because if you re implanting the cochlea then you are implanting stereocilia cells If you give someone a cochlea his or her stereocilia cells are not the issue B is false because it just doesn t matter C is true because remember that certain areas of our brain are responsible for processing different stimuli If you don t use certain areas those areas can shrink Use it or lose it Individuals that have not heard in many years will have more difficulty to adjust and be able to hear compared to a little kid When sound wave hits it goes in the middle ear and hits the bones Once it gets in the cochlea it will bend the stereocilia mechanicallygated K channels and they will allow potassium to in ux Once in uxed it depolarizes the cell causing the voltagegated calcium channels to form vesicles and NI are exocytosed to the ligandgated afferent neuron Party Room and Review Session Exam 4 Serotonin impacts mood Histamine impacts consciousness The more synapses the more complex the response For 33 on practice exam A is true because action potentials are never bidirectional they are always bidirectional The axon s midpoint is in the middle of the axon meaning that if you impact it can go both ways and the node that got impacted will hyperpolarize so that the signals go away and not back to that node Action Potential Steps 0 Membrane at rest 70 Vm and both gates are closed 0 Local depolarization reaches threshold potential and voltagegated Na channels open Na in ux causes more depolarization positive feedback Na channels become inactivated and K channels open Repolarization begins and Na channels close Cell hyperpolarized due to slow closing of K channels 0 K channels close and the cell returns to rest ACh goes from presynaptic to postsynaptic Big things are cognition Biogenic amines are neurotransmitters like ACh Naturally at rest there is more potassium inside the cell and more sodium outside the cell Vm Z equilibrium potential The different potentials o Graded potential local change in the voltage of the membrane which is caused by a change in ion ow What kind of stimulus would cause those channels to open Ligandgated or mechanically gated The local change in voltage by opening ligand or mechanically gated channels Positive is DEPOLARIZATION and more negative is HYPERPOLARIZATION 0 Temporal summation one presynaptic ring signal doing it over a short period of time 0 Spatial summation two or more presynaptic neurons send signals at the same time 0 First thing that happens when you reach threshold voltagegated sodium channels open In ux of sodium causes it to become more depolarized This opens the potassium channel to repolarize it go back to rest It order to hyperpolarize you need the potassium to ow OUT What is the signi cance of the hyperpolarization from K The action potential is unidirectional 0 Both graded and action potentials are electrical If you don t have myelin your sodium can leak out Action potentials aren t affected by distance because of positive feedback There are no channels in the myelinated sections 0000 Action potentials will all look the same graded potentials can vary which is why subthreshold potential exists Action potential is always graded potential but graded potential is not always action potential For 31 Exam 4 calcium is needed to form vesicles so you can exocytose so that you can pass signal from presynaptic to postsynaptic So removing the calcium would decrease it You need neurotransmitters to actually pass the message on What the brain receives is the number of neurotransmitters You re going the opposite direction of where you want to go by hyperpolarizing therefore you are decreasing it Explain when one neuron is telling the post to depolarize and another one is telling it to hyperpolarize The hyperpolarize will affect the depolarizing ACh delivers from presynaptic to postsynaptic The graded potential will be caused by ligand or mechanically gated channel Action potential cannot cross that In other words the action potential gets converted to ACh in order to cross Example of a presynaptic factor 0 You need something to help you send the message across neurotransmitter 0 You need calcium gt vesicles 0 You need receptors to receive the signal to start the action potential 0 You need membrane potential you need to stay depolarized being hyperpolarized will prevent all this from happening Example of postsynaptic o Receptors o Membrane potential you have to stay depolarized once again 0 Calcium is involved in the release of the neurotransmitters You need them to move the vesicles or exocytose Relationship between brainstem and digestion 0 Brain stem regulates the openings make sure air goes to lung and that food goes to the stomach Drinking alcohol can damage the myelin making the communication of action potentials slower Hence the slurred speech and slowed re exes White matter of the brain is closer to the inside white is a bunch of axons In the spinal cord the white matter is closer to the outside Spinal cord injuries are dangerous because they impact the axons of the white matter since they are more exposed In a normal cell it is more negative inside Thalamus regulates motor control Diencephalon includes thalamus Forebrain includes diencephalon What exactly is membrane potential when talking about pre and postsynaptic Once neurotransmitter makes it to dendrites of the next neuron The thalamus controls motor ACh biogenic amines dopamine serotonin histamine Any time an ion is moving through the membrane whether hyper or depolarized can affect the membrane potential Threshold potential is simply a level An action potential is NOT a threshold potential Exam 3 Party Room 2614 End result of JAK kinase they create ion channels and proteins It is an enzyme binds to a receptor which changes shape which then activates the JAK kinase not the actual kinase which the activates the JAK kinase which synthesizes proteins which then connects to an ion channel or protein If you want to decrease expression of an intracellular receptor An antagonist you catabolize it in order to decrease expression of an intracellular receptor Agonists create the same reaction Antagonists do the opposite Speci city has to do with shape and charge Take that away and nothing can bind Nonpolar ligands cannot move to the polar region without some Amphipathic protein moving it that s the plasma binding protein Afferent neurons do NOT have dendrites They receive neurotransmitters from a presynaptic causing it to re off Effector protein can either be an ion channel or an enzyme If it s an enzyme it ll cause something to happen inside the cell If membrane bound receptor is an ion channel the ligand can just drop down into the cell JAK kinase will ALWAYS result in protein synthesis Tyrosine kinase simply will activate proteins Exam Review Session Sodium concentration is higher outside the cell We pump Na from outside the cell to inside the cell and potassium from inside the cell to outside the cell 0 We need an ATP bound to the channel and as soon as the Na bounds to the channel it will hydrolyze The ATP then turns into ADP and phosphorus The ADP leaves but the phosphorus stays inside the cell When the potassium binds the phosphorus gets knocked off 0 There are three sodiums out and two potassiums in Osmolarity example 0 You have 2 Mng 3 NaCl 2 Glucose and 2 L of water Osmolarity 7 o 2 Mg 4 Cl 3 Na 3 Cl 2 glucose divided by 2 142 Osmotic Pressure 0 If both the solvent AND solute are permeable then there is no osmotic pressure 0 If the solvent is permeable but the solute is not the side with the most solute will expand and the side with the less amount of solute will shrink o If neither is permeable then the entire thing will expand in snze o In general water will go from a low solute concentration to a high solute concentration so that the ratio can be even 0 EVERYTHING diffuses from high to low in respect to itself water to water solute to solute otherwise it will be the oppos e Electron transport chain 0 The main objective is to make ATP 0 Oxygen is necessary for it to run Oxidative phosphorylation is necessary but since oxygen isn t present you resort to substrate level phosphorylation o The product from glycolysis and the Krebs cycle are essential for the electron transport chain The important byproducts from the Krebs cycle are the H and NADH enzymes which are carriers for H The H are carried by NADH to the area where electron transport chain happens in the mitochondria You have a big matrix area in the middle and an area with lots of folds and all the H and NADH are moving to the outside of the matrix and you are using the H to pump electrons into the folds of the mitochondria The cycle is NAD to Krebs cycle to NADH to Electron transport chain The important thing to keep in mind is that you NEED the byproducts from glycolysis and the Krebs cycle in order to run the electron transport chain properly 0 Study what the products are before and after each of these processes o Krebs cycle needs oxygen INDIRECTLY o If oxygen weren t present the electron transport chain would shut down rst and when the NADH doesn t have an electron transport chain to drop off all the H then they will shut down causing a domino effect which will then affect the Krebs cycle Three types of junctions 0 Tight junctions No interstitial OR intracellular ow 0 Gap junctions Allows the ow of intracellular uid within more than one cell and the movement of interstitial uid through the outside of the cell 0 Desmosomes There is no intracellular ow but interstitial uid can still ow between the cells For question 27 go to party room 0 C no osmotic pressure change correct answer 0 Hyper or hypo is about solute concentration Nonpolar ligands after they cross the membrane to the inside of the cell will bind to an intracellular receptor Go to party room for question 29 Oxidative phosphorylation is where you make the most ATP The Krebs cycle makes much less Glycolysis o Glucose cytosol 10 NZ 2 ATP Krebs Cycle 0 Mitochondria location 0 2 ATP H C02 0 NADH and FADH Electron Transport Chain 0 34 ATP H20 CON8 heat
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