* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download 1 Biology 13100 Problem Set 7 Components and functions of all
Nervous system network models wikipedia , lookup
Development of the nervous system wikipedia , lookup
Subventricular zone wikipedia , lookup
Patch clamp wikipedia , lookup
Single-unit recording wikipedia , lookup
Membrane potential wikipedia , lookup
Action potential wikipedia , lookup
Neurotransmitter wikipedia , lookup
Resting potential wikipedia , lookup
Biological neuron model wikipedia , lookup
Signal transduction wikipedia , lookup
Chemical synapse wikipedia , lookup
Feature detection (nervous system) wikipedia , lookup
Electrophysiology wikipedia , lookup
Neuromuscular junction wikipedia , lookup
Neuropsychopharmacology wikipedia , lookup
End-plate potential wikipedia , lookup
Synaptogenesis wikipedia , lookup
Molecular neuroscience wikipedia , lookup
1 Biology 13100 Problem Set 7 Components and functions of all nervous systems Master regulation of development in plants and animals depends on patterns of responses to signals that are shared among very different kinds of organisms. One of the earliest systems to develop in most animals is the nervous system. Sensory neurons (afferent neurons) transmit information from sensory cells to the central nervous system (CNS) whereas autonomic and motor neurons (efferent neurons) transmit information from the CNS to muscles, glands, and organs (effectors). Interneurons transmit information from sensory to motor neurons and between other interneurons within the CNS. Spinal and cranial nerves transfer information to/from specific tissues. Regions of the cerebral cortex have a receptive field and are responsible for certain functions (the sensory and motor homunculus). To understand how this system works, remember that cell membranes have ion channels. Some are ligand-gated. Others, called voltagegated channels, open and close with changes in the cell membrane potential. A membrane will become more permeable if ion channels open, but the flux of ions across a membrane depends not only on the concentration gradient but also on the electrical membrane potential. A neurite is an extension of a neuron (a nerve cell). It may later become either an axon or dendrite. A ganglion is a collection of nerve cell bodies (the part of the cell with the nucleus). During development, neural crest cells collect in ganglia near the spinal cord (the dorsal root ganglia) and send out neurites to the periphery and to the spinal cord. These sensory neurons convey information to CNS. Motor neurons have their cell bodies in the ventral part of the spinal cord and send long neurites to the muscles. They are not derived from neural crest cells. In order to form axons, the cell body sends out neurites and these can grow long distances to find their targets. The end of the neurite has a growth cone, which explores the environment and selects the direction of growth. We can generate normal human neurons from stem cells and they survive transplantation but we have no idea how to promote accurate axonal outgrowth to long distance targets. Human stem cells can come from four sources: embryonic stem cells (ESCs), nuclear transfer of unfertilized cell cells (or other types of gene transfer), direct infusion of transcription factor proteins to convert a cell to a stem cell, or other forms of transdifferentiation. One example of transdifferentiation would be to convert bone marrow cells into myocytes and coronary cells that line the walls of a blood vessel. A stem cell is an undifferentiated cell found in a differentiated tissue that can renew itself (replicate) and differentiate to give rise to all the specialized cell types of the tissue from which it originated. It is important to note that scientists do not agree about whether or not adult stem cells may give rise to cell types other than those of the tissue from which they originate. An important and useful property of stem cells is that of self-renewal (replication). Similar signaling pathways may regulate self-renewal in stem cells and cancer cells. In fact, cancer cells may include ‘cancer stem cells’ — rare cells with indefinite potential for self-renewal that cause growth of tumors. A stem cells glossary for biol13100 is online at https://wiki.bio.purdue.edu/biol13100/index.php/Stem_cells_including_cancer#Glossary 2 Properties of excitable cells Electrical signals are used to transmit information within cells through changes in membrane potential (Vm). Depolarization is an increase in Vm relative to resting Vm and Hyperpolarization is a decrease in Vm relative to resting Vm. Neuron cells communicate via two basic forms of electrical signals: graded potentials (small amplitude, short-distance signals) and action potentials (APs): larger amplitude, long-distance signals Action Potentials. An AP is a large and rapid (1-2 msec) all-or-none change in Vm involving depolarization of the membrane due to changes in permeability of the membrane to ions and currents carried primarily by sodium and potassium ions via voltage-gated channels (voltage-gated ). The AP uses energy stored in the membrane potential. What occurs with regard to ion movements (currents) is due to diffusion via specific ion channels, and different specific ion channels open during each phase which is reflected in membrane permeability changes as follows: 1. upswing (depolarization): voltage-gated Na+ channels open by positive feedback (activation gate opens), Na+ influx makes Vm increase 2. peak of AP: just before the peak, voltage-gated Na+ channels have started to close (inactivation gate closes) and voltage-gated K+ channels have started to open, so both K+ efflux and Na+ influx are occurring; thus, peak approaches but does not reach the Eeq for Na+. 3. downswing (repolarization): all voltage-gated Na+ channels are closing, all voltagegated K+ channels are open, K+ efflux dominates 4. after-spike hyperpolarization: all voltage-gated Na+ channels are closed and inactivated, all voltage-gated K+ channels are open, K+ efflux brings Vm below resting Vm (hyperpolarizes) 5. return to resting Vm: inactivation gates of voltage-gated Na+ channels begin to open but activation gates close, voltage-gated K+ channels are closed, cell returns to resting conditions Only cells with a resting nonequilibrium Vm and voltage-gated Na+ and K+ channels can generate and propagate APs. These are called excitable cells. Excitable cells exhibit a refractory period when the membrane is “refractory” to stimuli – no AP can be generated in response to the same stimulus. A refractory period is composed of the Absolute Refractory Period and Relative Refractory Period Speed of AP propagation along the cell depends on how far in advance of the point where the AP is present does the current spread to bring the membrane to threshold. Speed may be increased by increasing the amount of current flow within the cytoplasm relative to the amount of current flow across the cell membrane. A squid giant axon does this by having a large diameter so it has more cytoplasmic volume relative to the amount of membrane surface area, thus increasing the proportion of current flow in the cytoplasm relative to the current flow across the cell membrane. Vertebrates increase AP speed by increasing the membrane resistance by “insulating” it with a myelin sheath made of many layers of cell membrane from another cell. The layer of cells that wrap around the myelin sheath, creating many layers, are called Schwann cells. Schwann cells are derived from Neural crest cell origins. Myelination results in saltatory conduction of APs between Nodes of Ranvier. 3 Transfer of signals between cells within the nervous system at synapses Most neuron-neuron junctions in nerve networks do NOT contain gap junctions through which APs are propagated between cells. Instead, at chemical synapses between a pre-synaptic cell and a post-synaptic cell, chemical messengers (neurotransmitters, NTs) must be used to communicate between cells. There is a synaptic delay of 0.5 - 1 msec for transmitting signals between cells. NTs are produced in the cell body, enclosed in membrane-bound vesicles, and transported to the axon terminals, where the vesicles await the appropriate signal for release. There are up to 100,000 synapses within the CNS; Only one type of neurotransmitter is released at a given synapse but different receptors can cause different neurons to respond to the same NT in different ways. (See powerpoint table for types of neurotransmitters). At the axon terminals, depolarization of the axon terminal membrane, due to AP propagation, opens voltage-gated Ca2+ channels located there, thus causing exocytosis and secretion of the NT vesicles into the synaptic cleft. The NT diffuses to the post-synaptic cell membrane and binds with specific receptors. NT-receptor binding results in opening or closing of specific ligand-gated (or chemical-gated) ion channels in the post-synaptic cell membrane, allowing a change in ion flux across the membrane and changing Vm (e.g., synapse between a motor neuron and a skeletal muscle cell). An increase in Vm = depolarization = excitatory post-synaptic potential (EPSP), whereas a decrease in Vm = hyperpolarization = inhibitory post-synaptic potential (IPSP). These are graded potentials; the magnitude change is proportional to the amount of ion flux resulting from NT-receptor binding. Enzymes rapidly degrade neurotransmitters so signal stops relatively rapidly (e.g., acetylcholinesterase). The net result on the post-synaptic cell is determined by spatial and temporal summation of PSPs . If the axon hillock reaches threshold, an AP is generated and propagated along the post-synaptic cell. A given cell may receive hundreds of synapses, from many different cells, and may allow convergence and divergence, or inhibition. The somatic motor system Spinal motor neurons control skeletal muscles. Cell bodies of motor neurons are in the ventral horn of spinal cord. Only one neuron from the spinal cord has the effector skeletal muscle (once this motor neuron is stimulated to initiate an AP, it propagates along the cell to the muscle). All somatic motor neurons release ACh at axon terminals, which binds to nicotinic AChRs. All synapses with skeletal muscles are excitatory (neuromuscular junctions): Motor neuron releases ACh, binds to nicotinic AChRs, causes excitation and contraction of muscle with this mechanism for activation of muscle contraction: 1. start at the neuromuscular junction, with the arrival of a motor neuron AP 2. AP to the terminal button (axon terminal) near motor-end plate 3. Voltage-gated Ca2+ channels open, Ca2+ influx 4. Release of ACh from vesicles 5. ACh diffuses across synaptic cleft 6. ACh binds to ACh-gated Na+ K+ channels on muscle 7. Muscle cell membrane depolarizes 8. Voltage-gated Na+ channels open, generating a muscle cell AP Note that skeletal muscle is specialized to respond only to ACh. It responds only by contracting. Unlike cardiac or smooth muscle, there are no adrenergic receptors in skeletal muscle. 4 Skeletal Muscle Excitation-Contraction Coupling Muscles are grouped according to antagonistic pairs, e.g. extensors/flexors. Whole muscle is made of many multinucleated muscle cells (muscle fibers), composed of myofibrils and myofilaments (with actin and myosin contractile proteins). A motor unit includes the muscle fibers connected to a single motorneuron. To get larger force production, more motor units are recruited, more individual fibers contract. Muscle fibers contain myofibrils, composed of myofilaments that include thick filaments with myosin and thin filaments with actin. For force production, the sarcomere shortens in response to cross-bridge formation; shortening of entire myofibril is achieved by increasing degree of overlap of thick and thin filaments in each sarcomere. The muscle cell membrane, called the sarcolemma, extends with a Transverse tubule system to spread the action potential into cell interior where it comes in close proximity to the sarcoplasmic reticulum to trigger release of calcium. The sarcoplasmic reticulum, like the endoplasmic reticulum of other types of cells, has calcium pumps that take up free Ca2+ from the cytoplasm. Remember that cells generally have a very low concentration of Ca2+ in the cytoplasm. When a motor neuron releases ACh at neuromuscular junction, it binds the Nicotinic AChR, a ligand-gated cationic channels that can be blocked by toxins/drugs. The action potential spreads through the sarcolemma to the T-tubule system where a voltage-sensitive protein on T tubules (dihydropyridine receptor) changes conformation. Somehow, this opens Ca2+ channels of the sarcoplasmic reticulum (SR), causing release of Ca2+ from sarcoplasmic reticulum into the cytoplasm. Intracellular Ca2+ rises and opens more Ca2+-gated Ca2+ channels of the SR. When intracellular Ca2+ rises, it binds to troponin C of thin filaments; Ca2+ plays a key role in initiating/terminating contractile events by causing a shape change in the troponin-tropomyosin complex. In the non-contractile state, the troponin-tropomyosin complex shields actin sites from binding myosin. However, when Ca2+ binds to troponin complex, specifically troponin C, topomyosin undergoes conformational change to reveal myosin binding sites on actin. If activated, myosin head binds to actin and pivots, causing filament sliding, sarcomere shortening, and muscle fiber contraction. The sliding-filament theory of contraction explains how this happens by formation of crossbridges by myosin heads. At a molecular level, you should know myosin structure to understand how the myosin ATPase works. The myosin head binds ATP and it hydrolyzes ATP, but ADP + Pi remain attached; this activates the myosin head for binding to actin. When the myosin head can bind to actin, ADP + Pi are released, the myosin head rotates, and the power stroke moves actin toward center of A-line. Then new ATP binds to myosin, myosin detaches from actin and the cycle repeats if ATP and Ca2+ available. Receptive Fields and Lateral Inhibition in the Visual System Unlike a motor neuron that releases ACh, the neurotransmitter released by a photoreceptor is glutamate. Its release always declines in response to light. Bipolar cells are the post-synaptic cells. Two types of bipolar cells have different receptors for glutamate, so that a reduction in glutamate causes opposite reactions. In one case, the bipolar cell depolarizes, and in the other, it hyperpolarizes. 5 In general, the physical area of the primary sensory cells to which a neuron responds is called the receptive field. In the case of the visual system, the receptive field of a neuron in the visual pathway is the area comprising the photoreceptors whose stimulation by light leads to a detectable response in the neuron, generally a change in the rate of firing action potentials. The Hermann-Hering grid illusion shows how receptive fields work. It consists of dark illusory spots perceived at the intersections of horizontal and vertical white bars viewed against a dark background. The dark spots originate from processing by cells in the retina. Perception depends a lot on assessing local differences in illumination as demonstrated by this example. Think of retinal organization as consisting of two major systems: the through system and the lateral system. Starting with the photoreceptors, the through system connects to the retinal ganglion cells via the bipolar cells. There are two lateral systems that are produced by the horizontal cells and the amacrine cells. These lateral networks give rise to the surround organization of receptive fields as seen in the retinal ganglion cells. The information from the retina is sent to the brain by the axons of the retinal ganglion cells. There are several different classes of retinal ganglion cells that differ in their response characteristics. The two classes are the ON and OFF which will be discussed below. The Hermann-Hering Grid Consider the receptive field of a ganglion cell in the retina. The field can be mapped by impaling a ganglion cell with a microelectrode, to record its membrane potential (and thus its action potentials) and then stimulating the photoreceptor cells by shining light on different areas of the retina. When those experiments were done, it was found that the receptive fields of ganglion cells are concentric circles of photoreceptor cells and the circle for a ganglion cell is centered on the ganglion cell. Some are activated when photoreceptors detect light, while others are activated in the absence of light. These two types usually encircle each other and are spread throughout the retina creating receptive fields. It was also found that there are two types of ganglion cells in terms of their receptive fields. One type, the on-center ganglion cell, is maximally stimulated when a spot of light is place at the center of its receptive field, and is strongly inhibited if an annulus of light, with the center dark, is shined on the receptive area. The other type, the off-center ganglion cell, is maximally stimulated (that is, maximally increases its rate of firing action potentials) if an annulus of light is shined on the receptive field, and is maximally inhibited if a spot of light shined on the receptive field. This organization can be understood in terms of the bipolar cells that connect the photoreceptors to the ganglion. The on-center ganglion cell is connected to the photoreceptors in the central spot by ON-bipolar cells and to the surrounding annular region via OFF-bipolar cells. The situation is reversed in the case of the off-center ganglion cells. The next Figure illustrates the two arrangements. Only a few of the photoreceptors that feed into a ganglion cell are shown. 6 It is important to understand that this arrangement of receptive fields is completely dependent on the existence of two kinds of bipolar cells and the function of those two kinds of cells. ON-bipolar cells depolarize in response to the hyperpolarization of the photoreceptor cells to which they are connected, and they pass on the depolarization to the ganglion cells, which causes increased rate of action potentials. OFF-bipolars, on the other hand, hyperpolarize in response to photoreceptor hyperpolarization (photoreceptors ALWAYS hyperpolarize in response to light) and pass that hyperpolarization on to the ganglion cells, which causes reduced rate of action potentials. Using ONCenter receptive fields as an example, when your eyes are focused on the Hermann grid (except at an intersection) the dark surrounding photoreceptors counteract the activity of the light center photoreceptors. The axons of the ganglion cells form the optic nerve. They make synapses in the lateral geniculate nucleus (LGN) of the thalamus. LGN neurons also have receptive fields arranged in concentric circles, but they have better contrast between the center and the annular areas. Convergence of the ganglion cells on the LGN cells leads to a sharpening of the receptive fields. LGN neurons project to simple cells of the cerebral cortex via stellate cells, and most simple cells have rectangular receptive fields. Almost all simple cells demonstrate spatial selectivity, meaning that they respond most strongly to rectangles of light in a particular orientation. This occurs though the convergence of adjacent circular receptive fields of the LGN cells onto one simple cell. For further detail, see Neural Control of Vision at http://web.mit.edu/bcs/schillerlab/research/A-Vision/A.htm Problem Set 7 1. Suppose that you have in culture an isolated motor unit from a vertebrate; that is, an intact motor neuron and its associated muscle fiber. If you were to replace the Ringer’s solution in which the motor unit was bathed with a Ca-free Ringer’s solution, what would you predict the effect would be on the functioning of the motor unit? For example, could you elicit an action potential in the neuron by stimulating it with a current source? Would the muscle fiber contract in response to an action potential? Explain your predicted result. 2. The snake toxin, bugarotoxin, binds to nicotinic ACh receptors and irreversibly blocks the binding site on the receptor for ACh. What would be the effect of bungarotoxin on the isolated motor unit described above? Would the muscle contract if the neuron were stimulated? Why or why not? (Note: the use of various toxins has proved exceedingly valuable for the study of ion channel physiology. The toxins have often been engineered through evolution to have an astonishing degree of specificity for a particular ion channel, sometimes for a subtype of a particular channel.) 3. The puffer fish toxin, tetrodotoxin (TTX), completely blocks voltage gated sodium channels, thus it blocks the generation and propagation of action potentials in neurons. Suppose the motor unit describe above were bathed in TTX so that stimulating the neuron did not cause 7 an action potential, thus preventing the neuron from secreting ACh at the synapse. If you added ACh (it is a readily available chemical) to the bathing medium, would this cause the muscle to contract? Why or why not? 4. Ouabain is a plant alkaloid that inhibits the Na-K ATPase. What would you predict the effect on action potentials to be if ouabain were applied to a neuron? (Hint: remember what was mentioned early in the course about the relative number of ions that cause electrical changes and that cause changes in ion concentrations.) 5. Describe the ionic basis for a typical action potential, including all steps (in sequence) that occur in an action potential (including the subsequent refractory period): what happens in terms of ion flow across the membrane (which ions, which direction, when), conductance (or permeability) changes, alterations in membrane gated ion channels. Also be able to discuss what would happen if, at any specific time during the action potential (AP), alterations were made to intra- or extra-cellular concentrations of specific ions, gated channels were blocked or opened sooner than normal (consider several different scenarios that you create). 6. Explain why the Nernst potential for Na+ can closely predict the peak amplitude of an action potential. 7. Explain the importance of voltage-gated Na+ channel inactivation (closing of the inactivation gate) for an AP and for the refractory period. 8. Explain why APs are called “all-or-none” electrical signals. 9. Explain what graded potentials are. 10. Explain how an action potential is propagated in an unmyelinated nerve and in a myelinated nerve. 11. Explain the difference between APs and post synaptic potentials, both of which are changes in membrane potential. 12. The equilibrium potential for Ca is +130 mV and that for K is -100 mV, in a typical mammalian neuron. Which type of ion channel would most likely underlie a hyperpolarizing IPSP response? Give your rationale. 13. Explain how EPSPs and IPSPs are generated in a post-synaptic membrane, and how both temporal and spatial summation occur. If a neuron receives an IPSP of -20 mV and an EPSP that is +35 mV that are spatially and temporally close to each other, would the resulting integrated response be a negative or positive response? What would happen if the two responses occurred at places in the neuron that were long distances from each other? 14. Would a drug that blocks the reuptake of a neurotransmitter have a potentiating or inhibiting effect on the synaptic response to that neurotransmitter? Give a rationale for your choice. 15. Explain convergence and divergence in neuron networks, and the significance of each. 16. List the components of a reflex arc and relate them to how the nervous system maintains homeostasis for the whole organism. 17. Explain why information about the strength of stimulation to a neuron cannot be encoded in the size of the action potential. How is the information encoded? 18. Suppose that an action potential is started simultaneously at two different places on an axon. Describe the propagation of the two action potentials. 19. A newly discovered element, Purduonium, exists in solution as a monovalent cation, Pm+. It is found that the concentration of Pm+ in neurons is 10 mM and the concentration in the outside solution is 1 mM. If a neurotransmitter opens a Pm+-specific channel in the neuron, is that neurotransmitter inhibitory or excitatory in this situation? Why? 8 20. Explain why the depletion of ATP following the death of an organism leads to rigor mortis, the stiffening of all of the skeletal muscles. 21. Consider the preparation described in Problem 1 above. What could you do to the Ringer’s solution that bathes the neuron in order to alter the amplitude of the action potential? 22. Shown in the diagram below are three cross-sections of a sarcomere. Identify the location of each cross-section within the sacromere Admin! 3/31/09 12:05 PM Comment: I am unsure where these arrows are pointing, or if the third image is an arrow? I think it is, and maybe if I studied more I should be able to figure it out…. 23. If you touch a very hot skillet, your hand jerks away before you sense the pain of the burn. Explain. 24. A certain (fictional) bacterial toxin inhibits the cGMP-specific phosphodiesterase. What would be the effect of the toxin on vertebrate photoreceptor cells in the dark? In the response of photoreceptors to light? (By the way, cGMP-specific phosphodiesterase inhibitors do exist. Viagra is such an inhibitor.) 25. Retinal is the molecule that actually absorbs light in rod cells and all three types of cones. How, then, do different cones respond to different wavelengths of light? 26. If the rhodopsin molecules in each of 10 rod cells absorbs one photon of light at about the same time, a perceptible flash is sensed by the brain. This is the lowest level of light that produces a detectable signal in the mammalian visual system. Assuming that the light is green (say, 500 nm), how much energy is imparted to the system by the absorption of the ten photons? How does this energy compare to the energy required to lift a 1 Kg mass 1 meter against gravity? [The energy required to lift the mass is equal to the work done. Work and energy have the same units, Joules (1 Joule = 1 Kg m2/s2). The work done is equal to force times distance, and the force required is equal to mass times acceleration of gravity (g ≈ 10 m/s2).] 27. What is the receptive field of an on-center ganglion cell? An off-center ganglion cell? 28. Describe the receptive field of the simple cells in the visual cortex. Explain how the simple cell receptive field arises from the convergence of inputs from cells with concentric receptive fields. 29. This graph was generated by students in a physiology lab. The top trace shows contraction force of a frog leg muscle, the bottom shows the electrical stimulus. What is happening to the 9 muscle and why? 30. You are a member of a team of scientists that recently discovered a previously unknown animal species, which is not a mammal. You have been assigned the task to determine whether a given motor efferent system in the animal is functionally similar to or different from that in humans using any combination of the following tools to find out if it works like the motor efferent system to a skeletal muscle cell (motor neuron - muscle fiber). Are the neurotransmitters and receptors at the neuromuscular synapse in this animal the same as in the human system? Experimental tools: for adrenergic receptors: EPINEPHRINE is an agonist of all types of adrenergic receptors DRUG H is an agonist of beta1-adrenergic receptors SALBUTAMOL is an agonist of beta2-adrenergic receptors CARMINE is an agonist of alpha-adrenergic receptors PROPANOLOL is an antagonist of both beta1- and beta2-adrenergic receptors PHENOXYBENZAMINE is an antagonist of alpha-adrenergic receptors COMPOUND Q is an antagonist of beta2-adrenergic receptors for cholinergic receptors: SUCCINYLCHOLINE is an agonist of nicotinic cholinergic receptors MUSCARINE is an agonist of muscarinic cholinergic receptors CURARE is an antagonist of nicotinic cholinergic receptors ATROPINE is an antagonist of muscarinic cholinergic receptors for ion channels: 10 DRUG A blocks ligand-gated Ca2+ channels within the muscle plasma membrane DRUG B blocks ligand-gated Na+ channels within the muscle plasma membrane DRUG C blocks ligand –gated K+ channels within the muscle plasma membrane DRUG D blocks ligand-gated Cl- channels within the muscle plasma membrane DRUG E blocks ligand-gated Na+/K+ channels in the muscle plasma membrane other tools you may use: use RADIOACTIVELY LABELLED IONS of any type ALTERING THE EXTRACELLULAR CONCENTRATION of any ion VIAGRA inhibits phosphodiesterase AEQUORIN fluoresces in the presence of free Ca2+ FLUORO-X fluoresces in the presence of free Na+ PEPTIDE-K fluoresces in the presence of free K+ Describe the experiments you would do, using any of the above tools, to answer the question completely (is this animal similar to the human?). First state how the system works in humans, for comparison (what is the neurotransmitter and receptor type at each synapse, and what happens when the receptor binds the neurotransmitter, in humans?) Be sure to include in your answer a description of the experimental set-up or design and the appropriate controls. If you need help, you may want to consult a library to find research publications where these drugs were used in experiments with muscle. 31. Explain in detail ONE specific effect, within the specified cell type, of a mutation in the gene that codes for ONE of the following (A or B); assume that the mutation renders the gene product nonfunctional. Then describe ONE thing you could do to counteract that effect on the cell (other than replace the gene, mRNA, or protein it codes for). A. cell membrane voltage-gated Ca2+ channel in a skeletal muscle fiber B. calmodulin in a multi-unit skeletal muscle C. Ca2+ATPase in a skeletal muscle cell Vocabulary for the BIOL13100 lectures related to Problem Set 7 absolute refractory period acetylcholine actin action potential adrenergic receptor axon axon hillock axon terminal bipolar cell brain 11 Ca2+ channels Ca2+ pump Ca2+ release channels central nervous system (CNS) cerebral cortex cGMP contraction convergence cross-bridge cycling dendrite depolarization dihydropyridine receptor divergence excitable cell excitation-contraction coupling excitatory neuron excitatory post-synaptic potential (EPSP) excitatory signal extensor fatigue flexor ganglion glutamate graded potential hyperpolarization inhibitory neuron inhibitory post-synaptic potential (IPSP) inhibitory signal integration of signals interneurons lateral inhibition LGN ligand-gated M line membrane potential motor end plate motor neuron motor unit motor unit muscle muscle fiber muscle shortening myelinated axon myosin Na+ channel inactivation Na+/K+ channel 12 Na+/K+ pump nervous system neurite neuron neurotransmitter nicotinic receptor OFF-bipolar cell Off-center receptive field ON-bipolar cell On-center receptive field opsin optic nerve perception permeability phosphodiesterase photoreceptor photoreceptor phototransduction pigmented epithelium postsynaptic receptor presynaptic terminal receptive field receptor reflex relative refractory period relaxation repolarization retina retinal cones retinal rods rhodopsin rigor mortis saltatory conduction sarcolemma sarcomere sarcoplasm sarcoplasmic reticulum Schwann cell sensory neuron Sliding filament theory sodium permeability spinal cord synapse synaptic cleft synaptic vesicle T-tubule 13 thick filament thin filament transducin trigger zone tropomyosin troponin voltage-gated voltage-gated Ca2+ channel voltage-gated Cl- channel voltage-gated K+ channel voltage-gated Na+ channel