PDBIO 305: Exam 1 Study Guide
PDBIO 305: Exam 1 Study Guide PDBIO305
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This 23 page Study Guide was uploaded by Kirsten Notetaker on Wednesday September 28, 2016. The Study Guide belongs to PDBIO305 at Brigham Young University taught by David Thomson in Fall 2016. Since its upload, it has received 24 views. For similar materials see Human Physiology in Physiology and Developmental Biology at Brigham Young University.
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Date Created: 09/28/16
PDBIO 305 Exam 1 Study Guide All the notes for this exam in one place, for your convenience Human Physiology - Introduction Physiology = study of body function Anatomy = study of body structure We study function, but function is still very dependent on structure! Body Organization Systems, layers of tissue organization, etc. Although we call a muscle muscle tissue, there are actually many types of tissue within an actual muscle besides muscle tissue Homeostasis – maintenance of a constant internal environment Relies on feedback – responses made after change has been detected Negative or positive Negative feedback is primary type of homeostatic control Opposes an initial change Components: sensor, control center, effector Sensor – monitors magnitude of a controlled variable Control center – compares sensor input w/ set point Effector – makes a response to produce a desired effect Positive feedback – not as common as negative Amplifies an initial change *Note: Important to be specific in this class! I.e. “oxygen” vs. “air” Teleologically speaking = what was the purpose of something happening? Ex: We breath harder when exercising because we need more oxygen Mechanistically speaking = what caused it to happen? (how did it happen?) Ex: Increased levels of carbon dioxide are detected by sensory receptors, which signal to the brain the need for more oxygen. The brain in turn signals the lungs to breath faster and/or deeper. In this class we usually speak mechanistically Chemistry Review Key: p+ = proton(s), e- = electron(s), amu = atomic mass unit Number of p+, neutrons & e- determine properties of an element Molecular weight: weight of a molecule relative to H atom Ex: H20 = (1.01 amu x 2) + 16 amu = 18.02 amu Bonds Ionic – transfer e- Newly created positive and negative atoms stay bonded because they attract each other, even though e- stays transferred Covalent – share e- Hydrogen – unequally share e- Ex: In H20 oxygen is more electronegative, so it pulls e- from two H atoms strongly Polarity within the molecule, and different molecules are attracted when their negatively polar & positively polar sides come close Peptide bond – hydrogenation of amino acids Moles Standard unit for the amount of a substance Standard unit: a certain number of items which does not change, i.e. 1 dozen 23 1 mole = ~ 6 x 10 molecules 1 mole H = 1 gram Easy way to calculate 1 mole of a molecule: Add total amu of atoms in molecule -> that many grams is 1 mole (because H is 1 amu) In other words total amu for any given element or molecule = # grams in 1 mole of that element or molecule Solutions = mixtures formed by dissolving one substance in another Solute = dissolved substance (i.e. salt) Solvent = substance in which the solute is dissolved (i.e. water) Molar solutions In physiology we want to know the # of molecules or ions in solutions This is expressed in molar base units (denoted by capital M – M does not mean mole!) 1 molar (M) = 1 mole/liter Mole = # of molecules, Molar = concentration (these are different!) Mole = molecular weight in grams Molar base unit = moles of solute per liter of solution (not solvent) To make a molar solution, can’t just add 1 liter of water to a mole! This would = more than 1 liter of solution Put mole in first and then add solvent to add up to 1 liter total Molar solution practice: How would you make 250 ml of 1M NaCl? 1 M NaCl = 1 mol (58g) NaCl /1L = 1000 ml .25 x 1 M NaCl = 14.5 g NaCl /250 ml How would you make 450 ml of 2.5M NaCl? 2.5M NaCl = 2.5 x 58 g = 145g NaCl /1L .45 x 2.5M NaCl = 65.25g NaCl/450 ml How would you make 1 L of 100 mM (millimolar = millimoles/liter) NaCl and 1 M glucose (MW = 180 amu)? 100 mM = .1 M 58 g x .1 = 5.8 g (5.8 g NaCl + 180 g glucose)/1 L Percent solutions = grams of solute in 100 ml solution (not in 1 L!) Ex: we prepare a 10% sucrose solution by weighing out 10 g of sucrose and then diluting to 100 ml w/ water mg% = mg solute/100 ml solution Ex: blood glucose concentration 100 mg% = 100 mg glucose/100ml blood Practice Example: 500 ml of NaCl contains 5g NaCl % solution = 1% (5g/500ml = .01 g/ml = 1%) mg% = 1000mg% (1% g/ml x 1000 mg/g = 1000mg%) Molar = 0.172 M (10g/L, 1 mole NaCl = 58g, 10g/58g = 0.172 M) (5g = 1 mole/58 g = .086 moles/500ml = .000172 moles/ml x 1000ml = .172 moles/L = M) Millimolar = 172 mM (0.172 M x 1000 mM/M = 172 mM) Metabolism ***FOR EXAM it is most important to know basic concepts along w/ reactants, products & enzymes/cofactors and where things happen – specific intermediate steps are not as important. Make sure to know how much of each product is produced from each step (glycolysis, Krebs/Citric Acid cycle, etc. for a given amount of a certain reactant!*** ATP (Adenosine Triphosphate) – cellular energy currency Made from adenine, ribose & 3 phosphate groups ATP Hydrolysis fun fact: every day you turn over (breakdown & resynthesize) an amount of ATP roughly equivalent to your body weight! Cellular movement, molecular synthesis, & transport across membranes all require ATP Phosphocreatine (PCr) creatine kinase Creatine phosphate + ADP -> <- creatine + ATP Able to produce ATP very quickly! ATP Production from Glucose: Glycolysis -> Citric acid (Krebs) cycle -> oxidative phosphorylation Glycolysis 10 separate sequential chemical reactions that break down glucose into 2 pyruvate molecules Anaerobic process Occurs in cytosol of cell Not very efficient – low energy yield Glucose -> 2 pyruvate + + Uses 2 NAD and 2 ADP + 2 P -> 2iNADH + H (to be used in oxidative phosphorylation) and 2 ATP Mitochondria and ATP production Pyruvate converts to acetate -> Acetyl-CoA -> citric acid cycle -> Occurs in mitochondrial matrix Mitochondria Energy organelle Major site of ATP production Contains enzymes for citric acid cycle & e- transport chain Enclosed by a double membrane Linking step Converts pyruvate (3 carbon) to acetyl-CoA (2 carbon) + + Pyruvate + CoA + NAD -> acetyl CoA + CO + NADH 2 H Krebs Cycle For each acetyl-CoA proceeding through the cycle: produces 1 ATP (GTP), 3 NADH, 1 FADH , a2d 2 CO 2 Does not require molecular oxygen, but will stop if oxygen is not available to the e- transport chain (ETC) Pyruvate from glycolysis is converted to acetyl-CoA which enters citric acid cycle Cycle consists of eight reactions directed by enzymes of mitochondrial matrix Important in preparing hydrogen carrier molecules for entry into ETC Total produced so far (from glycolysis & Krebs cycle): 4 ATP, 10 NADH, 2 FADH2, 6 CO2 Electron Transport Chain (ETC) – mechanism of oxidative phosphorylation NOTE: this is mostly a reference to help understand the overall process, remember you don’t need to memorize each of these reactions Requires oxygen Series of reactions on the inner mitochondrial membrane Major source of ATP 1 H released by earlier rxns is carried to inner mitochondrial membrane by NADH or FADH and r2leased a NAD is free to pick up another H 2 A “high energy” e- is extracted from the H and passed along from protein to protein, releasing energy as it moves to a lower-energy state + 3 This energy is used to pump H (generated in step 2) from the matrix to the intermembrane space a Creates an electrochemical gradient + 4 At end of ETC oxygen recombines w/ H -> H O 2 5 Proton gradient generated in step 3 has stored energy – protons want to travel down from high-energy state in intermembrane space back into the matrix, where energy state is low + a Occurs through a H ion channel called ATP synthase 6 ATP synthase uses energy released as protons flow through it to generate ATP from ADP and inorganic phosphate 7 NADH drops its H and associated e- off at complex I and results in the release of enough energy for production of ~2.5 ATP 8 FADH drops its H and associated e- off at complex II. This is downstream from complex I and thus less energy is released, fewer protons are pumped into the intermembrane space, and fewer ATP (~1.5) are generated Uncoupling proteins (UCPs) insert in th+ inner-mitochondrial membrane and act as a channel through which H can be transported Basically steals H from ATP synthase -> decreased ATP production Protein & fat are oxidized in similar ways Protein -> amino acids -> Krebs cycle -> oxidative phosphorylation, etc. Fat oxidation Fats are stored as triglycerides (glycerol + 3 fatty acids) Lipolysis = breakdown of triglycerides Fatty acids separate from glycerol Glycerol can enter glycolysis Beta-oxidation = Fatty acids (many carbons) -> acetyl CoAs (2 carbons) This then enters the Krebs cycle -> oxidative phosphorylation, etc. Typical fatty acid is 12-14 carbons in length, so many Acetyl CoAs are produced from 1 fatty acid molecule This occurs in the mitochondria “Anaerobic” Glycolysis Normal glycolysis is actually not ever aerobic (using oxygen), but “anaerobic” glycolysis refers to the glycolysis which happens when oxygen supplies are limited (which affects the ETC) When oxygen is limited, the ETC gets backed up and NADH levels increase because they can’t enter the ETC -> decrease in NAD + levels Decrease in NAD -> Krebs cycle can’t go, so it stops -> buildup of acetyl CoA and pyruvate Decrease in NAD also -> glycolysis can’t go, so it also stops Lactate dehydrogenase uses NADH + H to convert pyruvate -> lactate This converts NADH -> NAD , which can now be used to continue glycolysis + This is less efficient because the NAD must be used again for the pyruvate conversion, so it does not go to the Krebs cycle and less ATP is produced – but this process can still happen quickly in response to oxygen deficiency This process is not indefinite, as the pH will decrease (conditions become more acidic) – eventually you will need to begin aerobic glycolysis again, but this helps while oxygen is limited Gluconeogenesis Creation of “new” glucose Amino acids, glycerol, lactate, are used as substrates for glucose formation Basically the reverse of the ATP production process Protein synthesis Know basic types of cells and their functions i.e. skeletal muscle cells vs. red blood cells The proteins of a cell determine its form, which determines its function Different proteins -> different functions Proteins are made in the nucleus from DNA “blueprints” DNA is made up of millions of nucleotides and replicates itself during cell division Note: don’t need to know structure of nucleotides T pairs with A and G pairs with C Gene = stretch of DNA that codes for the synthesis (creation) of a specific polypeptide or protein Unique base sequence for each protein Every 3 bases code for one amino acid Protein synthesis – see slide on Learning Suite, make sure you understand the process depicted Transcription – occurs in Nucleus RNA Polymerase binds to DNA and separates it, reads it, and forms a complementary strand of mRNA Translation – occurs in the cytoplasm Ribosomes read the mRNA and put together a protein chain based on the mRNA code Ribosomes Contain a little RNA (called rRNA) which allow them to recognize the mRNA The Leader Sequence – determines where the newly translated protein will go Leader sequence = sequence of base codes at beginning of protein strand which are recognized by wherever the location is they need to go (sequence is different for different locations) After translation protein is folded, leader sequence is cut off, etc. to form finished protein Occurs in endoplasmic reticulum and Golgi apparatus Membrane Transport Concentrations of various solutes are different on the inside vs. outside of the cell Movement of stuff across the cell membrane is regulated 2 major molecular driving forces Chemical: due to a concentration gradient Electrical: due to an electrical gradient Taken together, these are referred to as the electrochemical gradient (ECG in these notes) Diffusion: NET movement of molecules or ions from an area of high concentration to an area of low concentration Passive vs. Active membrane transport Transportation requires some sort of force (energy) to move the particles across the membrane If the process requires the cell to expend energy, then it is active transport Carried out by proteins called pumps If the process does not require the cell to expend energy, then it is called passive transport Driving force is the electrochemical gradient IMPORTANT: passive transport does still require energy, as all objects require energy in order to move (basic physics) – passive means that the cell as a whole does not need to expend energy (because it is moving with the gradient) **NOTE** There will be a question on the test about this! Be sure not to answer “true” for a true/false question that says “Ions do not use energy to move in passive transport” or similar Passive transport Simple diffusion Through lipid bi-layer or through channels Facilitated diffusion Carrier-mediated (binds to something in the membrane which helps it through) Active transport Primary active Carrier-mediated – same as with passive but in this case ATP must be used to activate the carrier Secondary active Carrier-mediated There is also tertiary and quaternary, but we won’t deal with those as much Vesicular transport (endo- or exocytosis) Fick’s Law of Diffusion Defines the effect of factors that influence the rate of diffusion across a membrane Factors that increase rate of diffusion Increased concentration gradient Increased permeability of membrane to substance Increased surface area of membrane Factors that decrease the rate of diffusion Increased molecular weight of substance Increased distance through the membrane Diffusion across a membrane Molecules/ions can diffuse through a membrane if it is permeable to that substance Permeability is determined by size of molecules/ions, presence of carriers or channels, charge of carriers/channels and molecules/ions, etc. Osmosis Special case of diffusion Net diffusion of water down its own concentration gradient through a semi-permeable membrane Osmolarity (osM) = the total solute particle concentration (as opposed to molecular (molar) concentration) To determine this, account for the fact that salts dissolve in water For the purposes of this class, if Cl is in the molecule it’s a salt Ex: 100 ml water contains 3 g KCl = 0.402 M Now in water, KCl dissociates into 2 different particles, which now creates twice as many particles (moles) in the solution Thus, in this solution KCl is 0.804 osmolar (multiply molarity by 2) Tonicity = osmolarity of a solution in relation to osmolarity of body fluids Isotonic = osM same as cells No uptake or loss of water from cells Hypertonic = osM > cells Cells lose water & become crinkled in appearance (crenation) Hypotonic = osM < cells Uptake of water by the cell causes lysis (bursting) of cells Hemolysis = lysis of red blood cells Pure water is hypotonic Channels vs. carriers Channels simply let ions through the membrane, while carriers actually change conformation to let an ion bound to it into the other side Carrier-mediated transport Specificity – most carriers will only transport 1 specific substance Competition – some substances compete for carriers Ex: glucose & galactose are close enough in structure to compete for same carrier binding Saturation – how much of the substance is present Rate of transport will increase with saturation until it is saturated enough that the carriers can’t work any faster and they are all being used Cotransport Symport (cotransport) A carrier moves multiple substances in the same direction Antiport (countertransport) A carrier moves multiple substances in opposite directions Facilitated diffusion – carrier-mediated passive transport Primary active transport Phosphate group from ATP binds to carrier & its negative charge changes structure (configuration) of protein carrier Substance bound to carrier is pushed to other side of membrane, after which it is released, the phosphate group is released & the protein changes back to original structure Sodium-Potassium ATPase Major player in many cells of the body Crucial for maintaining ion concentration in many cells + + Basically a pump to maintain Na and K levels in the cell + 1) A pump bound to Na us+s a phosphate from ATP to change shape and push the Na out of the cell + 2) The pump then binds to K which is outside the cell and gives up its phosphate in order to change back to its original shape and release the K inside the cell Secondary active transport Ex: epithelial cells of intestine Mechanism for glucose absorption from gut to blood Vesicular transport Material is moved into or out of the cell wrapped in membrane Active method of membrane transport Two types of vesicular transport Endocytosis – moving into the cell Exocytosis – moving out of the cell Provides mechanism for secreting large polar molecules Enables cell to add specific components to membrane Membrane Potential Membrane potential = separation of opposite charges across plasma membrane Plasma membrane of all living cells has a membrane potential (polarized electrically) Due to differences in concentration and permeability of key ions When MP exists, the unbalanced charges will accumulate in a thin layer along the membrane Measured in voltage Equilibrium potential is the voltage (membrane potential) at which concentration gradient = electrical gradient Net transfer of ions stops Nernst equation – memorize this equation and know how to use this to calculate equilibrium potential! E K 62 log ([K ] /BK ] )A E K equilibrium potential (this is assuming physiological temperature conditions) Measured in mV (millivolts) + [K ] B potassium ion concentration on side B (in mM) + [K ] A potassium ion concentration on side A (in mM) By convention, in physiology the inside of the cell is the reference side (side A) The answer (E ) is the charge on side A K If the membrane is only permeable to one ion the Nernst potential (membrane potential) for than ion represents the total membrane potential We can change the sides of (+) and (-) charge by changing the permeability of the membrane Changes permeability allows different ions to come through, which creates different equilibrium potentials See slides for examples Calculating total membrane potential (V ) m Composite of individual Nernst (membrane) potentials for each ion for which the membrane is permeable Greater the permeability (conductance, g) of the membrane to any one ion, the greater the contribution of the Nernst potential for that ion to the total membrane potential If a membrane is not permeable to any ions, those ions do not affect the potential Goldman Hodkin Katz Equation (know this equation too!!) Vm= [(E )Kg )K+ (E )Na )]Nag K + g) Resting Membrane potential in the cell Na-K pump creates ion gradients (low Na, high K inside cell) Resting membrane potential is due mainly to the diffusion of K down its concentration gradient from inside the cell to outside through leak channels Na diffusion into the cell through its leak channel counteracts this, but its effect is very small because a cell at rest is not very permeable to Na Changes in Membrane potential Polarization = any state when the membrane potential is other than 0 mV Depolarization = MP becomes more positive Repolarization = MP becomes more negative (but still more positive than resting membrane potential) Hyperpolarization = MP becomes more negative than resting membrane potential At rest cell membranes are polarized (usually ~ -70 mV) So this is usually the baseline (resting membrane potential) Two types of potentials Graded potentials = local change in membrane potential (short- distance) Action potentials = long-distance signals Graded potentials Small change in membrane potential Triggered by opening or closing of gated ion channels Gates open in response to stimuli picked up by sensory receptors -> depolarization Magnitude of the graded potential depends on magnitude of the triggering event In other words, a bigger stimulus = bigger graded potential Spread by passive current flow – adjacent areas also depolarize when positive current reaches them Decremental = magnitude of current decreases the further it spreads (these do not spread far) Graded potentials do not actually cause a nerve to “fire” (send a signal to the brain) unless the current reaches the axon hillock Action Potentials Rapid, large change in membrane potential Conducted over entire membrane Magnitude does not diminish as it moves (it is NOT Decremental) Potential moves from -70 mV to about +30 mV, then back down Threshold In order to create an action potential, the stimulus must produce a graded potential change which reaches threshold (about -50mV) If threshold is reached, it will always produce an action potential This can also happen through summation (adding) of graded potentials Temporal summation – graded potentials happen in quick succession & build on each other enough to reach threshold Physical/spatial summation – graded potentials happen relatively close by each other & combine to reach threshold Channels – summary Na -K pump: active transport, pumps Na out of the cell and K into + the cell + + K diffusion channel: passive diffusion of K out of the cell + + Na diffusion channel: passive diffusion of Na into the cell + + Voltage-gated Na channel: allows Na into the cell during the depolarization of an action potential Voltage-gated K channel: allows K out of the cell during the repolarization of an action potential There is actually not very much movement of ions during an action potential, it only takes a few ions to cause a single action potential Na -K pumps restore balance of ions after the action potential All or None Law Excitable cells respond to a stimulus with a maximal response or none at all – size in not related to the strength of the stimulus In other words, an action potential is the maximal response of the cell and will always occur if threshold is reached but will never occur if threshold is not reached Graded changes (EPSP & IPSP) can occur in the cell body of neurons – these are NOT all-or-none Lidocaine Diffuses into the neuron & binds to voltage-gated Na channel Prevents Na channel from opening in response to voltage changes -> no action potential, even if graded potential reaches threshold -> no nerve transmission to central nervous system (CNS) Absolute Refractory Period Around the time of depolarization & repolarization Sodium gates are open or sodium inactivation gates are closed (sodium gates are not reset) & potassium gates are open In other words, sodium gates are not at rest During this time another action potential cannot be produced, regardless of the size of stimulus, because channels are already open & cannot open further, or inactivation gates are close & will not open Relative Refractory Period Around the time of hyperpolarization & returning to baseline Sodium gates are reset by potassium gates are still open During this time another action potential can be generated, but only with a stimulus larger than usual This is because potassium is still leaking out of open channels (which close sluggishly), which causes the membrane potential to go more negative and thus requires a greater stimulus to get to the necessary threshold Contiguous conduction Action potential can move forward along axon from hillock to terminal Potential begins at one site, which then moves to nearby sites and creates an action potential there, etc. until potential has been propagated along entire axon However, this must occur in only one direction (forward & not backward) so that one stimulus does not continuously cause action potentials for an indefinite period of time Due to the refractory period, sites that just had an action potential cannot have another one directly afterward Thus sites adjacent to the first site won’t end up re-stimulating the first site, and instead only stimulate sites further down the axon This is the type of conduction for unmyelinated axons Myelination Basically insulation for the cell – decreases membrane permeability where axon is myelinated (meaning those myelinated sections won’t depolarize) Schwann cells myelinate cells in PNS, oligodendrocytes myelinate cells in CNS Gaps in axon that are unmyelinated are called Nodes of Ranvier Voltage-gated channels are concentrated highly in these nodes Saltatory Conduction Action potentials are propagated about 50x faster than in contiguous conduction, because positive charge current “jumps” from node to node rather than moving along each site of the axon The Synapse Summary of nerve transmission so far: 1 Graded potentials occur on the cell membrane of the nerve 2 If they are big enough, or if enough occur simultaneously, the membrane is depolarized to threshold, setting off an action potential which spreads down the nerve axon Synapse = connection between two neurons Sequence of events in a synapse (helpful to draw it out for yourself) 1 Action potential d++olarizes presynapti++membrane 2 Voltage-gated Ca channels open, Ca enters presynaptic axon terminal 3 Ca ++triggers exocytosis of neurotransmitter 4 Neurotransmitter binds to receptor on postsynaptic cell membrane 5 Postsynaptic neuron responds 6 Neurotransmitter may be degraded by enzymes OR taken back up by presynaptic neuron OR diffuse away from synapse Chemically gated ion channels EPSP: Excitatory Post-Synaptic Potential Neurotransmitters cause depolarization of the postsynaptic neuron With channels that allow both K and Na through, + electrochemica+ gradient favors movement of Na inside the cell and inhibits K movements outside of the cell because the cell at rest is negatively charged IPSP: Inhibitory Post-Synaptic Potential + Channels open which only let K through, which moves out of the cell and hyperpolarizes the postsynaptic neuron There are other ways for IPSP to occur, but we won’t cover them in this class Whether an EPSP or IPSP occurs depends on the type of neurotransmitters Summation Temporal summation: adding together of EPSPs or IPSPs generated by firing of the same presynaptic terminal at high frequency Special summation: adding together of EPSPs or IPSPs generated by firing of two or more presynaptic neurons simultaneously These may cancel each other out, i.e. EPSP & IPSP adding together = no change Grand Postsynaptic Potential (GPSP) Composite potential on the postsynaptic membrane due to all EPSPs and IPSPs occurring at the same time Is the net change a depolarization that reaches threshold? “To fire or not to fire – that is the question.” If GPSP reaches threshold an action potential is generated at the axon hillock Central Nervous System (CNS) Glial cells Astrocytes – physically support neurons, regulate external environment around neurons Oligodendrocytes – form myelin sheaths in CNS Microglia – phagocytosis (immune defense) Ependymal cells – neural stem cells, aid in production of cerebrospinal fluid Protection & nourishment of CNS Skull & vertebral column protect brain & spinal cord Meninges of the brain Dura mater – thick outer membrane Arachnoid mater – webbed middle membrane Pia mater – thin inner membrane Cerebrospinal fluid Cushions brain, exchanges nutrients with interstitial fluid of brain Produced by ependymal cells of choroid plexuses Circulates through ventricles & central canal, then into subarachnoid space at 4 ventricle Empties from subarachnoid space into sinuses through arachnoid villi Blood-brain barrier Blood flow to brain is principally through carotid arteries Blood-brain barrier tightly regulates substances that are allowed access to brain cells Consists of endothelial cells of brain capillaries Astrocytes important in getting epithelial cells to form tight junctions (instead of gap junctions like most capillary epithelial cells) CNS is composed of the brain and spinal cord 3 parts of the brain Forebrain – cerebrum & diencephalon (thalamus, hypothalamus, & pituitary gland) Conscious thought, memory, emotion, etc. Cerebellum Motor coordination, balance Brainstem – midbrain, pons, & medulla oblongata Many involuntary, basic functions Functional areas of the cerebral cortex – know the general functions of each area (don’t need to know where they’re found) Primary motor cortex Voluntary movement (carries out “orders” from premotor cortex) Premotor cortex and supplementary motor area Generate plans for movement Coordinate complex movements (i.e. movements involving many different muscles) Somatosensory cortex Cutaneous (skin) sensation (touch, temperature, pain) & proprioception (awareness of where your body is relative to the surrounding environment and space) Posterior parietal cortex (sensory association areas) Perception of where the body is in relationship to the environment (proprioception) Works with premotor cortex to guide movements toward targets Primary auditory cortex Perception of sound Primary visual cortex Perception of sight Parietal-temporal-occipital association cortex Integrates sensory information (light, sound, touch) Important in determining what it all means Prefrontal association cortex Personality Reasoning & planning (conscious) Creativity Decision making Limbic association cortex Motivation Emotion Memory & learning Thalamus & basal nuclei (AKA basal ganglia) Nucleus = a functioning group of cell neurons Thalamus Relay station for sensory information – screens out unimportant info Relay station for motor pathways from cerebral cortex Interpretation center for sensory information Modality of sensation (pain, heat, cold, touch pressure) is perceived here, but not location or intensity Basal nuclei Inhibition of muscle tone Coordination of slow, sustained movements (especially posture) Selecting purposeful patterns of movement and suppressing useless patterns of movement (filtering the multitude of signals coming from the brain) Cerebellum Spinocerebellum Regulation of muscle tone Coordination of skilled voluntary movement Motor cortex tells cerebellum what to do at the same time it sends command to muscles -> muscles sent info about what movement was actually carried out to spinocerebellum -> spinocerebellum makes adjustments as necessary Cerebrocerebellum Planning and initiation of voluntary activity Vestibulocerebellum Maintenance of balance, control of eye movements Tremor Resting tremor – tremor when no movement is intended Parkinson’s is a resting tremor that can actually be temporarily improved with intentional movement Destruction of dopaminergic neurons in the basal nuclei (substantia nigra) leading to excess muscle contraction Symptoms include resting tremor, increased muscle tone (rigidity), decreased voluntary movement Intention tremor – jerky voluntary muscle movements due to failure of the cerebellum to dampen the motor functions when you are intending to move in a specific way Huntington’s disease Caused by degeneration of the caudate nucleus Symptoms include chorea (Greek “dance”), released inhibition leads to quick, uncontrollable movements Even just sitting up or standing uses plenty of muscles and thus is not truly resting, so the tremor occurs then too Wernicke’s area Comprehension of language (both spoken & written) Formulating patterns of speech Broca’s area Articulation of speech Hypothalamus Regulates body temperature Regulates osmolarity of body fluids (intake & excretion of water) Regulates food intake (appetite & satiety centers) Emotions of rage & aggression Regulates anterior pituitary function (endocrine system) Regulates uterine contractility & milk ejection (via oxytocin) Regulates sleep/wake cycles Brain stem Cardiac center (medulla) controls heart rate & strength of contraction Vasomotor center (medulla) controls blood pressure Respiratory centers (medulla & pons) controls rate & depth of respiration Digestive center (medulla) controls vomiting, swallowing, coughing, sneezing
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