* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Physio study guide unit 2
NMDA receptor wikipedia , lookup
Neuroanatomy wikipedia , lookup
Synaptic gating wikipedia , lookup
Node of Ranvier wikipedia , lookup
Nonsynaptic plasticity wikipedia , lookup
Clinical neurochemistry wikipedia , lookup
Endocannabinoid system wikipedia , lookup
Nervous system network models wikipedia , lookup
Neurotransmitter wikipedia , lookup
Patch clamp wikipedia , lookup
Single-unit recording wikipedia , lookup
Action potential wikipedia , lookup
Chemical synapse wikipedia , lookup
Synaptogenesis wikipedia , lookup
Biological neuron model wikipedia , lookup
Membrane potential wikipedia , lookup
Signal transduction wikipedia , lookup
Electrophysiology wikipedia , lookup
Resting potential wikipedia , lookup
Neuromuscular junction wikipedia , lookup
Neuropsychopharmacology wikipedia , lookup
End-plate potential wikipedia , lookup
Study guide for Unit two; Lecture one: Membrane Structure and Function Chapter Readings: Chapter 2 and chapter 4 Cell Membranes (Ch 2 pg 12-14) 1. Describe the fluid mosaic model of the cell membrane. 2. Describe the chemistry of the phospholipids and the structure of the bilayer. Give the reason for the orientation of lipid molecules in the bilayer. 3. What other types of molecules are found in membranes and what are some of their possible functions? 4. Define selectivity (think channels) and semipermeability (lipid bilayer) with respect to the cell membrane. 5. Discuss the limitations that membranes generally impose on movement of ions and molecules. Membrane Transport (Ch 4) 1. What substances can cross the lipid bilayer easily and what substances have low permeability? 2. What is osmosis? If water is still moving across the cell membrane, but there is no NET movement because it is at equilibrium, is this osmosis? 3. What is osmotic pressure and what governs osmotic pressure—mass or number of particles? Why? 4. What is the difference between tonicity vs. osmolality? Which term will we use in class? 5. When we are concerned about net movement of water across cell membranes, are we worried about transient changes from permeant molecules or are we worried about changes from impermeant molecules? 6. What would an iso-osmotic or hyperosmotic or hypo-osmotic solution do to a cell? 7. Fact: the body fluid compartments have the same concentration. What is this magical number? Fact: the body fluid compartments have different compositions: why don’t these solutes simply diffuse? 8. Note the concentrations of sodium, calcium, and potassium inside and outside the cell. If these ions were suddenly allowed to move across the cell membrane, which way would they go? 9. Do all cells set up these gradients for these ions? Which cells can “tap” into this stored energy (like a battery) and use it to do work? 10. Describe the two types of transport: passive and active. 11. What sub-categories fall under passive transport? Describe their characteristics. 12. What factors govern the rate at which simple diffusion across a membrane occurs? 13. As another way of learning this material, try writing down all modes of transport: simple (lipid-soluble and water-soluble via channels); facilitated diffusion; and active transport (primary and secondary) which are carrier-mediated ? which require energy expenditure by the cell ? Define vmax. Which modes of transport can be saturated? 14. In what way(s) are simple diffusion and facilitated diffusion similar, and in what ways do they differ? 15. What is the energy source for active transport? Where, and by what processes, is ATP made? 16. What is secondary active transport? Identify the two types (co-transport and anti-port). How do they differ? In what way are they alike? 17. Plot the rate of transport of a substrate across a membrane at increasing substrate concentrations both for simple and facilitated diffusion. What is the significance of a Vmax? 18. Describe the action and energy requirements of the Na+/K+ pump. 19. How can the permeability of a membrane suddenly change? 20. What is a voltage gated channel vs. ligand gated channel? Give examples of ways that the opening and closing of a gate can be controlled. Membrane Potentials and Action Potentials—Chapter 5 and 45 Review the concentrations of sodium, chloride, calcium, and potassium intracellularly and extracellularly. Why is the inside of the cell negative? What is the membrane potential? Do all cells of our body have this potential? Which tissues can manipulate this potential to do work? What is resting membrane potential? Describe equilibrium potential—why is it a battle between electrical and chemical gradients? Why is the membrane potential generated by passive diffusion? To which ion is the membrane potential attributed to and why? Is any ion at equilibrium across the cell? Does active transport have any influence on membrane potential? If the cell membrane were more permeable at rest to sodium, than potassium, what would the resting membrane potential be like? Define: excitability, depolarization, hyperpolarization, overshoot, repolarization and threshold. If the permeabilities of sodium, potassium, and chloride were individually increased, in which way would the ions diffuse? What is threshold? (Remember, stating a voltage value is NOT a definition). What is the definition of an action potential? Can you identify/list some characteristics of action potentials? Why are action potentials important? What function(s) do they serve? Explain how action potentials rely on changes in permeability via voltage-gated channels that leads to passive diffusion. Can you draw an action potential curve? What constitutes the upstroke? Downstroke? Hyperpolarization? Can you label on this curve when certain channels are opening (that is, permeability to a certain ion has changed), and when they are closing (inactivating and/or deactivating depending on which ion you are discussing). Discuss conduction velocity: which types of neurons conduct action potentials faster? Do you know what is meant by “gating” of a channel and when a channel is in a conducting state vs nonconducting state? What are the three ways a channel’s conductance can change? Discuss sodium’s three gating positions. How are these gating positions involved in refractory period? What is absolute refractory period? What is relative refractory period? What is saltatory conduction (salta means “to jump”) with respect to myelination? How does myelination both increase velocity and conserve energy? What is the Pathophysiology behind multiple sclerosis? Can you draw a neuron, label its anatomical parts and draw what types of channels are found throughout the neuron? Note: on the dendrites, you SHOULD NOT limit yourself to just ligand operated sodium channels, right? The synapse is composed of five things: the presynaptic membrane, the synaptic vesicles within the terminal bouton, the synaptic cleft, the post-synaptic membrane and the ligand operated channels found imbedded in it. What roles do mitochondria play at the synapse (I discussed two!). What role does calcium and voltage operated calcium channels play for neurotransmitter release? Be able to discuss events occurring on a POST-SYNAPTIC membrane: EPSPs and IPSPs—which ion channels, if opened would generate these? Is a post-synaptic neuron likely to fire an action potential after one EPSP? Two? Ten? Twenty? Sixty? What is spatial vs. temporal summation? Discuss the design and function of the neuron: appreciate that the dendrites are the “receiving” end of the neuron and the terminal bouton is the “sending’ end of the neuron. Discuss how neurons communicate in a one-way fashion using both electrochemical means. Lastly, what are graded potentials vs. action potentials? Where would you find these events occurring on the neuron? Compare and contrast graded (local) potentials vs action potentials and be able to describe the experiments Hodgkin and Huxley performed to demonstrate these events. What happens when a stimulus depolarizes the cell at a certain spot, yet threshold is not reached? When is the Sodium/Potassium ATPase active in a neuron? What is its role in the neuron? What is its role in ANY cell for that matter? Neurotransmitters, Neurotransmitter receptors and Pharmaceutical influence of these Of the neurotransmitters discussed in class, be sure to know if a particular NT is excitatory or inhibitory and how they are degraded or removed from the synaptic cleft. Be sure to know how other drugs can augment or inhibit them, e.g., how is too much glutamate a bad thing for a neuron? What do benzodiazepines such as valium stimulate GABA-tropic receptors? What do MAO and MAOI’s do? Is it o.k. for someone to take an MAOI and ephedrine? Why? What does ecstasy do to SSR pumps? How is ACh synthesized? What is the role of AchE? Upon release of ACh into the synapse, what is the sequence of events that occur in the cleft and at the postsynaptic membrane? What two types of receptors can ACh bind to? What actions result from the binding of ACh at these two different receptors? How many ACh bind to an ACh receptor? What ion will flow through? What type of event would this trigger on a post-synaptic cell? What are Ionotropic receptors? That is, how do they work? Do we ONLY have ionotropic receptors that allow sodium through the channel? Which example of an ionotropic receptor are you responsible for knowing? What ion does it allow through? What are metabotropic receptors? That is, how do they work? Which two examples of metabotropic receptors do you have to know? Do they use the same second messenger? What effects will occur in the cell once a second messenger is activated? Be able to go through all the second messenger pathways and be able to describe the cell surface receptor, G-protein, effector protein, second messenger, late effector protein, and target protein. Agents that interfere with neural or neuromuscular transmission. (Covered in lecture and Ch 7) Describe the site and mechanism of action of each of the following substances. Curare Atropine (Belladonna alkaloids) Botulinum toxin Black widow spider venom DFP (di-isopropyl fluorophosphate) Neostigmine, physostigmine TEA Tetrodotoxin (TTX) Muscarine and nicotine as agonists for ACh receptors Sympathomimetic drugs Parasympathomimetic drugs Skeletal Muscle Contraction (Chap 6,7) Anatomy review 1. Be familiar with the organization of muscle (fascicle, fiber, fibril, etc) 2. Be familiar with the structure of the sarcomere (A,I bands, etc) 3. On your own, list all of the sequential events in neuromuscular transmission, beginning with a neuron, through the NMJ and then in muscle. Go through the excitation, EC coupling, and contraction steps in muscle, being as detailed as you can-- Describe the sliding filament theory, outlining the steps involved and describing the structure and function of each of the principal proteins: actin, myosin, troponin and tropomysosin. Describe the energy requirements. 4. How do T-tubules assure uniform excitation of all fibrils in a fiber? What is the role of the SR? 5. How does calcium get into the sarcomere, how is it removed, and what is its role there? 6. What changes in appearance occur to the sarcomere at the peak of contraction? 7. What is the appearance of the NMJ and the motor endplate? Name the two types of receptor to which ACh can bind at the EP membrane. 8. What is the name of the local potential produced by ACh action at the endplate? 9. How does the local event eventually become an AP? Muscle Mechanics (Chap 6 and 54) 1. Define and be able to graph a twitch. How much time does a single twitch take in skeletal muscle? 2. What is tetanus, and how is it produced? How can muscle contraction summate? 3. Define a motor unit. Do motor units differ in size? How? 4. What is the effect of stimulating motor units of different size? 5. Define recruitment of motor units. What is the effect of doing so? 6. What is a muscle spindle and what reflex is it a part of? What is a Golgi tendon organ and what reflex is it a part of? Spinal Reflex Arcs and Autonomic Nervous system questions 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. What is the role of a sensory receptor in neural pathways? Identify several different types of sensory input that you can receive. Differentiate between the somatic and autonomic branches of the nervous system. Which effector organs are innervated by each of these? Discriminate when the sympathetic vs. parasympathetic nervous systems are active. What does each division do to the eye, heart, G.I. tract, glands of the body, and blood vessels. Describe the localities of the preganglionic cell bodies for the sympathetic and parasympathetic nervous systems. Describe the localities of the postganglionic cell bodies for the sympathetic and parasympathetic nervous systems. Describe the effector cells of the sympathetic and parasympathetic nervous systems. State the types of neurotransmitters released from the sympathetic and parasympathetic nervous systems (from both the preganglionic and postganglionic cells). Where does the sympathetic nervous system use ACh? Explain why the adrenal medulla still adheres to the “two neuron chain rule.” State the overall effects mediated by the activation of the receptors used by the sympathetic and parasympathetic nervous systems. Reconstruct the second messenger pathway used by the receptors of the sympathetic nervous system. Where do you find alpha receptors and what do they cause when stimulated? Where do you find Beta receptors and what do they cause when stimulated. Reconstruct the activation of a parasympathetic nervous system receptor (both types!) Understand autonomic tone. How will the autonomic tone change if a person is given the following drugs (note, you should also understand what each drug does): Phenylephrine Isoproterenol (isoprenaline) Albuterol Ephedrine/ pseudoephedrine Amphetamine Reserpine Phentolamine (why use this for cocaine overdose?) Propranolol Nicotine Muscarine Pilocarpine Neostigmine/physostigmine Atropine (why use this in conjunction with epinephrine to increase heart rate and blood pressure ? Why use this to treat people who ingested muscarine?)