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Week 3 Notes

by: Rachel Sanchez

Week 3 Notes Biology 220

Rachel Sanchez
Human Anatomy and Physiology
Jennifer Doherty

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About this Document

Here is a complete week of notes discussing membrane potentials with necessary graphs and numeric values. It also goes through the neuromuscular junction, EPP, EPSP, and IPSP.
Human Anatomy and Physiology
Jennifer Doherty
Class Notes
biology 220, bio220, UW, Washington, huskies, Physiology
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This 10 page Class Notes was uploaded by Rachel Sanchez on Saturday October 17, 2015. The Class Notes belongs to Biology 220 at University of Washington taught by Jennifer Doherty in Fall 2015. Since its upload, it has received 55 views. For similar materials see Human Anatomy and Physiology in Biology at University of Washington.


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Date Created: 10/17/15
Week 2 Notes 10121016 Various Kinds of Membrane Potentials Type Generated by Found where Important when ENa No net ow Equal In all cells at the in magnitude for membrane This the concentration is only important and electrical in the case of the gradient driving forces EK Electrical and In all cells at the chemical gradient membrane This with arrows going is only important in different in the case of the directions No net driving forces ow Resting 1 Sodium Found in all cells Membrane Potassium This is always Potential pump important but 2 Leaky especially for Potassium cells not and Leaky undergoing any Na electrical channels signaling Threshold Stimuli or Found in all cells 55mV membrane This is important changes to send electrical occur and and chemical depolarize signals Cell the communication membrane is essential for to a point life until an action potential is propagated Membrane potential Voltage difference or separation across a membraneelectrical potential What creates a membrane potential Ions Separation of charged is referring to the membrane The blue box shows across the membrane there are different charges A potential is a gradient Resting membrane potential Managed and created by both Leaky channels and sodiumpotassium pump 0 For the pump 3 sodium ions move out and 2 potassium ions move in Which channel exists in greater amounts There are less LeakyNa and more LeakyK RMP is 70mV and if membrane potential is determined by charges and internal concentration of charge is dictated by ions then more potassium exists inside The driving force for sodium is in and potassium is outside Define equilibrium potential no net ux due to the equal Equilibrium Potential forces of diffusion 60 for Sodium Why Things to use in answer driving forces 0 Chemical forceelectrical force 70 RMP I Forces cancel one in and one out I Equal magnitude 90 for Potassium o The concentration force determines what the equilibrium potential is as seen in lab Nernst equation Used to find different concentrations 0 Regular EionRTZf ln ionoutionin o ENa60 and Ek90 RMP combination of both ions moving 0 More potassium leaving than sodium entering o If only one channel existed the membrane potential would move towards that ions equilibrium potential Practice problem Make a diagram of an action potential and be sure to label each ions part in it whether they have channels open and are they moving in or out of the cell The most important part of this problem is explain why each ions acts how they do 0 Must label properly what type of channel it is o Voltagegated sodium depolarizes the cell and exhibits positive feedback because more and more voltagegated sodium channels open They go towards ENa o Voltagegated sodium channels close they are quick channels and voltagegated potassium open These channels are slower to open and bring the membrane potential more negative 0 Hyperpolarization voltagegated potassium brings the membrane potential close to EK and then the cell is brought back to RMP Key Questions 1 What is important about having a larger amount of leaky K channels than leaky Na channels a What would happen if it were the other way aroundmore leaky Na 2 Predict and defend what would happen if all leaky sodium channels were blocked a Leaky K What if there were twice as many Na K pumps Explain the equilibrium potential for potassium Not the numerical value What kinds of molecules things have an equilibrium potential Would T4 have one 9195 Day 2 1013 How is the signal passed to nearby neurons 1 Initiated by stimuli Mechanosensitive channels all over the dendrites Stimulus changes membrane potentials and goes to threshold a Trigger zone enough sodium enters the channels and triggers Action Potentials 2 Propagate down the axon a Concentration stays the same because a large amount of ions would be required to change the amount a little bit 3 Diffuse into the synaptic cleft Clicker Question During an action potential the depolarization is affecting the driving forces During the middle of the action potential are sodium ions moving into the axon still What about near the top Also explain what is happening to the driving forces Answer Yes the middle point sodium is moving with the electrical and concentration gradient The top point is going against its electrical gradient but still has enough depolarization at the membrane to be with the concentration gradient If you didn t understand this question use the Flux Steps to organize your thoughts into rate in and rate out How are the driving forces reacting in or out Is the concentration gradient changingAre the membrane and channels related to conductance inversely displaying a lot of resistance Mohammad continued from Friday What could have caused his symptoms New Ideas 1 Ach breakdown is inhibited 2 Unable to synapse 3 Neurotoxin impacts CNS continuously signaling with action potentials 4 Botulism acts as a neurotoxin and originated from mulch outside the dentist s office Sodium channels are blocked How does an action potential get to the end of the neuron to synapse 0 Key term positive feedback 0 Opens one voltagegated sodium channel and sodium ions rush into the axon This increases membrane potential and depolarizes the voltagegated sodium channels next to the first one and this just keeps happening 0 Electrically positive charges enter and nearby negative charges are attracted to them and move away from the membrane This changes the membrane potential and opens more voltagegated sodium channels Why don t action potentials propagate up the axon The inactivation gate causes a refractory period where no action potentials can occur Why won t an action potential fire immediately after the end of the first one This is for two reasons 1 Hyperpolarization occurs in all action potentials and if this is occurring the membrane potential is going towards potassium s equilibrium potential at 90mV and getting an action potential to fire during this period means the stimulus needs to change the membrane potential ZOmV more than the normal action potential 2 The refractory period the inactivation gate acts like a plug and doesn t allow any more sodium to enter The gate is not voltage sensitive like the channel and so another action potential will not cause it to open until repolarization occurs a The plug inserts at 30mV Day 3 1014 What is the importance of the nucleus for cell communication The cell body is necessary to make neurotransmitters the sodiumpotassium pump and the channels Electrical signaling would not occur without these Where do synapses occur Neuron to neuron generally 0 Interneuron to motor neuron o Sensory neuron to interneuron 0 Motor neuron to muscle cell also called muscle fiber 0 interneuron to interneuron Note Receptors for nerve transmitters are often ion channels so they open They are ligandgated 3 steps for neurotransmission 1 Neurotransmitter release from presynaptic neuron 2 Receptor opens neurotransmitter gated 3 Neurotransmitter removal a Neurotransmitter either diffuse away are reuptaked by presynaptic cell or enzyme degradation b Must leave postsynaptic cell otherwise a signal would be continually sent In a muscle this means continued contraction Presynaptic membrane proteins voltagegated calcium channel sodiumpotassium pump voltage gated potassium leaky sodium leaky potassium For voltagegated calcium channel when an action potential depolarizes presynaptic membrane at axon terminal the voltage gated calcium channels open Calcium then enters because ux goes down its chemical gradient concentration gradient big electrical gradient cell is depolarized so high membrane potential The electrical gradient is not important in this case What happens at the presynaptic membrane After calcium enters o Snare protein complex is induced for membrane fusion 0 Synaptotagmin binds calcium and undergoes a conformational change 0 This protein complex pulls vesicle to fuse membrane 0 Synaptotagmin changes shape 0 This causes a shape change in snare shape and it fuses with membrane Acetylcholine The acetylcholine receptor will admit sodium and potassium ions as well 0 Receptor is a cation channel 0 When the receptor is open what happens to sodium and potassium I Sodium will enter and potassium will exit They are following the two driving forces Electrical gradient 0 Sodium in because negative membrane potential 0 Potassium going out o More sodium is leaving because of the gradient moving away from like charges 0 As long as acetylcholine Ach is available an EPSP will occur I Degradation occurs by acetylcholinesterase in the synaptic cleftquick reaction Choline portion of acetylcholine put back into the axon terminal and is used to make more acetylcholine I How is acetylcholine removed from the receptor By achE the enzyme The amount of acetylcholinesterase determines the magnitude of EPSP 0 Then the sodiumpotassium pump brings the cell back to RMP resting membrane potential I The size and time span of the depolarization caused by EPSPs are based on the amount of Ach being released into the synaptic cleft Determined by the number of action potential because this increases the rate that Ach is released from its presynaptic cell 0 Rate of Ach out of the postsynaptic cell determined by degradation I Skeletal muscle muscle fiber bundle myofibril made of sarcomeres made up thick and thin filaments anchored at mline myosin zline actin Sarcomeres shorten without thick or thin filaments changing length 0 Relaxed tropomyosin blocks myosin binding site on actin 0 Contract calcium binds troponin displaces tropomyosin conformational change 0 Calcium and ATP must be present I NM site of signal exchange end of presynaptic cell I When enough muscle fibers contract in unison they produce enough force Day 4 1015 Threshold Graded potential summation at dendrites in front of trigger zone and changes membrane potential if threshold is reached action potential is propagated 0 Not action potentials o Trigger zone top of axon where threshold is breached and action potential begins to propagate 0 Various synapses on the dendrites 0 Most neurons only release have one neurotransmitter EPSP excitatory o AchAcetylcholine channel it is a cation channel that lets in sodium and potassium upon depolarization o Increases membrane potential mV 0 time 0 IPSP inhibitory o GABA works just like Achbinds to receptors on postsynaptic membrane and opens channels to let in an ion I In this case not cation but chloride channels I Decreases membrane potential when membrane potential changes I Hyperpolarization chloride moves in from interstitial uid to cell 100mM outside and 5 inside mV time On a neuron receiving both Ach and GABA what happens to membrane potential 0 Current decays over a distance down axon and so the closer to the trigger zone the stronger the signal whether excitatory or inhibitory 0 Current ows it doesn t stay and wait to reach threshold Summation Threshold is at 55mV can summate below this but it won t generate an action potential Only minimal membrane potential changes seen Temporal summation Occur in timevarious membrane potential changes occurring close enough in time that the cell can not go back to RMP o Seen as a small change to an action potential then hyperpolarize then resting potential again 0 Temporal summation in a neuron is different than in a muscle Spatial summation sounds like it is SPACEial various neurons sending signals to another neuron ensuring the neuron raises above threshold Summation with and EPSP and IPSP if they occur in the same time frame they cancel out 0 Ex If an IPSP hyperpolarizes the membrane potential 15mV and an EPSP depolarizes 15mV or even 30mV the numbers will sum and still be below threshold Antagonistic pairs exor vs extensor They have opposing movements 0 Tricep extensor versus bicep exor 0 Stretch receptor tells the brain not to extend anymore 0 Messages sent to your motor neuron are sent at 25Hz because your muscle gets into tetanycontracting enough I Muscles not designed to just twitch o If stretch receptor signals nerve no muscle will not contract I This can be overcome by neural information o Sensory re ex if muscle is stretching too far a re ex will occur 0 Interneuron excitatory synapses with Inhibitory interneuron synapses with extensor o Interneuron excitatory synapses with interneuron inhibitory synapses with sensory and motor neuron for exor muscle 0 In this system if the inhibitory interneuron didn t work what would this mean Mohammad final Actual answer SNARE helps bind and release GABA if broken vesicles cannot fuse Tetanus toxin attacks SNARE but only on muscular interneurons that are interneurons o Muscles affected first have short motor neurons 0 Motor neurons are interactive Tetanus treatment 0 Antibiotics 0 Antibodies to bind tetanus immune globulin 0 Drugs to prevent spasms of muscles or to relax 0 Mechanical ventilation for lungs because paralysis or spasms could have occurred Day 5 1016 Anesthesia Aja Symptoms o Fever rigid muscle increased C02 in breath due to hyperventilation red face Cause of symptoms 0 In ammatory response 0 Allergic responseanesthetic o Anesthetic impact on motor neuron o Contraction increase because increased ATP I Decrease because of decreased ATP 0 Something preventing relaxation 0 Maybe calcium not taken from actin laments 0 Something With cellular respiration amount of C02 expired What structures would need to be included for a SMRF modeling explaining Aja s symptoms 0 actin o Lungs O mYOSin o Myosin binding 0 C02 0 calcium site on actin O T39tubUIeS 0 SR 0 Voltagegated O ACh 0 muscle bercell Channels 0 Cellular respiration 0 motor neuron 0 Oxygen m1tochondr1a o sympathetic o SNARES nerve o G AB A o troponin o tropomyosin o EPSP o IPSP 0 ATP Synapsing from one neuron to another 0 Neurotransmitter must bind to receptor 0 If enough binds to receptors and gets released threshold will be reached 0 Action Potential will then propagate in postsynaptic o What is the mechanism for synapsing from a motor neuron to a muscle fiber 0 25 sec tetany that will cause Ach release 0 Always releases enough Ach to trigger muscle contraction o EndPlate Potential EPP occurs at the neuromuscular junction 0 Occur because of neurotransmitter being released into a muscle fiber 0 When an endplate potential reaches threshold a muscle cell will propagate an action potential mm Otime 0 o Neuromuscularjunction o Voltagegated potassium channels also open at threshold 0 Sodium rushes in whereas potassium has its gate only slightly open and so depolarization 0 Once inside the muscle the rushing in of sodium causes a depolarization and then hyperpolarization 0 Below graph changes that occur in membrane potential after the neuromuscular junction mV vs time 40 l o What would happen if acetylcholine remained bound to the AchR 0 Muscle relaxation would be hindered o Uptake of calcium would not occur as fast as calcium release 0 Muscle anatomy 0 Inside of muscle cell AKA muscle fiber is myofibril and inside that is a sarcomere o Sarcoplasmic reticulum Ttubule o Mitochondria O Be able to find all this anatomy on different structures and know their job in the muscular mechanism


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