Neurophysiology Study Guide

Neurophysiology Study Guide 1. Define equilibrium dominance. Why is the resting capability closer to the kB equilibrium potential (EK+) than the atomic number 11 potential (ENa+)? The equilibrium potential is the point at which the force exerted on an ion by electrostatic and concentration incline forces atomic number 18 balanced, and on that point is no net movement of that ion. The resting potential is closer to EK+ than ENa+ because the cell tissue layer is more permeable to potassium than sodium. 2. How would ENa+ change following an change magnitude in the external concentration of sodium?Would the resting potential be affected significantly? If the external concentration of sodium was increased, the concentration gradient driving the movement of sodium would be increased more sodium would diffuse into the cell and would reduce some of the negative charge on the inner surface of the lipid bilayer. This would take to heart to decrease (make less negative) the resting po tential, save would non affect it significantly since the membrane is much more permeable to K. 3. Does any net Ionic current black market at the resting potential?What be the relationships among passive and coreionic currents at the resting potential? There is no net ionic current flow at the resting potential. However, since neither Na+ nor K+ is at equilibrium, there is a net flow of each across the membrane. The Na-K heart and soul generates the concentration difference that sustains the resting potential notwithstanding it is the passive ionic flow that creates the resting potential. Pump currents balance passive currents (diffusion) at the resting potential. 3. Define electrogenic and neutral pumps.What role does the Na-K pump play in the resting potential? An electrogenic pump creates a potential difference across the membrane positive and negative charges ar not transported across the membrane in equal amounts. Neutral pumps are balanced according to charge there is no potential difference created. The Na-K pump generates the concentration difference that sustains the resting potential. 5. Describe the sequence of ionic events and their effect upon the resting potential following lockade of the Na-K pump, or following an increase in extracellular potassium or sodium. When the Na-K pump is blocked by an agent such as oubain or digitalis, Na+ and K+ entrust continue to diffuse passively across the cell membrane down their respective gradients. After a while, intracellular Na leave alone increase and intracellular K will decrease. The reduced K gradient will reduce K efflux through nongated convey therefore, the resting potential will depolarize. The reduced Na gradient will have little effect on the resting potential.If extracellular K+ is increased, the driving force for potassium diffusion out of the cell will decrease, and the resting potential will become less negative (depolarized). If extracellular Na+ is increased, the driving forc e for sodium movement into the cell will increase with a pull up stakesant slight depolarization, but there will be no significant change in resting potential. Na+ -K+ ATPase pump activity Y Na+in Y Na+O/ Na+i Y ENa+ Y (EM ENa+) Y INa+ Y Conduction velocity and Depolarized threshold 6.excuse the interrelationships amidst ionic and capacitive currents during postsynaptic potentials or during an litigate potential. Ionic current is the flow of ions through conduct into or out of the cell. Capacitive current is the movement of charges, usually positive, up to or away from the cell membrane. During an excitatory postsynaptic potential or an march potential, there is an initial ionic current flow into the cell, followed by a capacitive current out of the cell, which serves to depolarize the membrane potential at a distance. The current twine forms a local circuit. 7.Define time continual. How is it calculated and why is it important for integration of electrical activity at th e axons initial segment? The time constant is the amount of time it takes for EM (membrane potential) to decay to 1/e of its initial strength (37%). It is equal to resistance times electrical condenser. It is important for integration at the initial segment because it determines whether temporal summation can take place a long time constant means slow decay which allows summation to bump a short time constant means fast decay, and therefore no summation. 8. Define length constant.How does it depend upon axon diameter, axial resistance and membrane resistance what does it suggest astir(predicate) the relative effectiveness of synapses on the soma versus synapses on the dendrites? The length (or space) constant is the distance that a signal can traveling before falling to 1/e (37%) of its initial magnitude. It is relative to the square root of the diameter of the roughage and to membrane resistance, and inversely proportional to axial resistance. The high the membrane resistanc e, the farther the signal will go. The larger the length constant, the slower the signal decay.This suggests that synapses on the soma are more likely to undergo spacial summation than dendritic synapses. 9. Define graded potentials. How do these differ from achievement potentials? A graded potential is one in which the amplitude is in a flash proportional to the magnitude of the foreplay. It has no refractory period and is a local potential i. e. it is not actively conducted and spreads barely passively. Graded potentials can be either depolarizing or hyperpolarizing and can add. serve potentials cannot add, have refractory periods are all or none, and are propagated actively. 0. Explain the ferment of a strength sequence curve. Define rheobase and chronaxie The shape of the strength-duration curve shows that initiation of an action potential is dependent on both the amplitude and the duration of a stimulus. Rheobase is the minimum effective stimulus strength. Chronaxie is the duration of the stimulus that is required to just reach threshold when the stimulus amplitude is twice rheobase. 11. Explain in detail how an action potential is generated. What types of take tend to exculpated as the membrane potential depolarizes?Draw a graph illustrating how sodium and potassium conductances change (with time) during an action potential. When the membrane is depolarized, voltage sensitive Na+ transmit open allowing Na+ to enter the cell down its electrochemical gradient This entry of Na+ further depolarizes the cell, resulting in the opening of more Na+ channels thus allowing more Na+ to enter, and so on. When the influx of Na+ exceeds the efflux of K+ , threshold is exceeded and the response becomes regenerative, leading to the depolarizing or rising phase of the action potential.After a period of time the Na+ channels inactivate and close blocking further entry of Na+ through these channels. Also after a delay, voltage-sensitive K+ channels open, allowi ng K+ to leave the cell, traveling down its electrochemical gradient. The inactivation of the Na+ channels coupled with the opening of the K+ channels result in the repolarization of the membrane potential 12. How do the time courses of sodium and potassium conductances differ during a maintained depolarization? A maintained depolarization causes Na+ inactivation (reduces PNa+) and hence increases (depolarizes) the threshold potential.In addition, compared with the Na+ activation process, the K+ activation process (increased PK+ ) is delayed and persists as long as the depolarization is maintained. 13. Define sodium inactivation. How does it explain the absolute and relative refractory periods, or accommodation? How do potassium ions play a role in these processes? What limits a neurons upper limit rate of firing? There are two gates on the voltage gated sodium channels. As the membrane is depolarized, sodium channels open. When the membrane is fully depolarized, sodium channels bec ome inactivated.Sodium inactivation is high at the peak of the action potential and is maximal about the time that the repolarization phase intersects the zero potential. It is this process and the position that most potassium channels are open that account for the absolute refractory period. The relative refractory period is the gradual recovery of Na+ channels from the inactivation process. Accommodation is also related to sodium inactivation because a slow depolarization will cause the Na+ channels to go directly from the closed state to the inactivated state. A neurons maximum rate of firing is limited by the absolute refractory period. 4. What role does the Na+ -K+ pump play in the action potential? How is the action potential affected by alterations in the concentration of extracellular Na+ or K+ Action potentials arise from the passive movement of ions down their electrochemical gradients. The Na+-K+ pump creates the electrochemical gradients that sustain the resting potenti al and generate the action potential. Alterations in the concentration of extracellular K+ will cause fluctuations in the resting potential that will decrease or increase the likelihood of an action potential being generated.Alterations of extracellular Na will increase or decrease the conduction velocity of action potentials as well as the likelihood of an action potential being generated. 15. Explain the mechanism for propagation of an action potential in an unmyelinated nerve or in a myelinated nerve. Why is the latter much windy? What factors affect conduction velocity? Once an action potential has been initiated, the inmost Na+ current depolarizes the membrane toward ENa+ . This results in a potential difference between this active locality and the adjacent inactive region, which is still near EK+ .Hence, current will flow between the active and adjacent inactive region, depolarizing the inactive region. The resulting increase in intracellular Na+ leads to an outward capaci tive current and depolarization of this region of membrane. When the depolarization reaches threshold, an action potential will be initiated in this region of the membrane. In an unmyelinated nerve, this is a continual process moving down the membrane. In a myelinated nerve, this process occurs only at the node of Ranvier. myelinated nerves have faster conduction velocities because the action potential jumps from node to node, which may be up to 2 mm apart.Conduction velocity is affected by membrane capacitance and by membrane and axoplasm resistances. Myelin increases membrane resistance, thereby constraining incoming positive charge to move down the axon. Myelin reduces membrane capacitance this reduces the amount of negative charge that must be neutralized to reach threshold. Axoplasm resistance is inversely proportional to axon diameter. Thus, conduction velocity increases with fiber diameter,. 16. Describe the process of saltatory conduction. Why is it advantageous? Explain ho w and why conduction velocity and the length (space) constant are affected by demyelinating iseases. Saltatory conduction is the noncontinuous propagation (jumping from one node of Ranvier to the next) of an action potential along a myelinated nerve. Saltatory conduction arises in part from the properties of the myelin sheath, which increases the membrane resistance and decreases the capacitance in the internodal region the result is an increase in current flow down the core of the axon. In addition the voltage-sensitive Na+ channels responsible for the extension of the action potential are localized only at the nodes.This type of conduction makes possible rapid precise control of muscle contraction. In demyelinating diseases conduction velocity and the length constant are reduced in the unmyelinated areas. The length constant is proportional to membrane resistance and when the myelin is destroyed, the resistance at that point decreases and therefore the length constant decreases. Because of increase capacitance and negative charge on the inner surface of the membranes, propagation of the signal takes place interminably instead of jumping from node to node therefore, conduction velocity is decreased. 7. What are the three functions of a sensory receptor? 1) Transduction of the environmental signal Energy Y Change in membrane potential 2) Amplification of the environmental signal 3) Transmission of the environmental signal to the CNS 18. How does a receptor potential or writer potential differ from an action potential? A receptor or generator potential is a graded potential that is proportional to the stimulus. It is not a function of the membrane potential and thus is not regenerative like an action potential.It has no refractory period and, therefore, is additive. It is local and propagated. Finally, the ion channels producing the receptor/generator potentials are different from those underlying the action potential they are not voltage gated. 19. Explain how an action potential is initiated in a sensory nerve. What conditions are necessary for repetitive firing? How does the firing frequency depend upon the amplitude of the generator potential? Upon the intensity of the stimulus? A sensory nerve action potential begins with the receipt of an appropriate environmental signal.The stimulus causes a localized increase in the permeability of the nerve remnant to Na+ . The resulting net inward positive ionic current depolarizes the nerve terminal. This current spreads passively along the axon terminal producing a depolarizing outward capacitive current The outward capacitive current, in turn. may induce an action potential in a region of the nerve with a low threshold for generating an action potential- usually at the first node of Ranvier in myelinated nerves. A maintained stimulus is necessary for repetitive firing.The firing frequency is proportional to the amplitude of the generator potential and the intensity of the stimulus. 19. De fine sensory adaptation. Name two classes of receptors. What type of information about the stimulus is derived from each? Give examples. Sensory adaptation is the descend in response that occurs over time when a receptor is subjected to a constant stimulus. There are two types of receptor classifications slowly adapting (tonic) receptors and rapidly adapting (phasic) receptors. behind adapting receptors provide information about the rate of change of a stimulus as well as the magnitude and duration.This type of receptor is seen in touch, pressure, pig cells for hearing and vestibular function, muscle spindle receptors, Golgi tendon organs and in baroreceptors. Rapidly adapting receptors are unable to maintain a free burning depolarization, despite sustained stimulation. They function as rate-detectors providing information about the rate of change of the environmental signal. Rapidly adapting receptors are found in the Pacinian corpuscles and skin hair receptors. 19. Describe in detail the steps involved in the leave office and degradation of ACh at the neuromuscular junction. What factors regulate how much ACh is released?Chemical synaptic transmission is initiated by a depolarization of the presynaptic element and the subsequent influx of Ca++ ions into the nerve terminal through voltage-dependent Ca++ channels. Ca++ facilitates contact of synaptic vesicles with the terminal membrane, which triggers the synchronous release of several thousands of transmitter molecules into the synaptic cleft. The ACh binds to its receptor on the postsynaptic membrane. After dissociating from the receptor, ACh is degraded by acetylcholinesterase (produced by ) 19. Define quantal release and miniature endplate potential.How are the two related? Quantal release refers to the release of neurotransmitters in discrete packets or vesicles. A single vesicle contains about 5-10,000 ACh molecules, and is capable of depolarizing the membrane about 1mV. The small depolarization ca used by the spontaneous release of a few vesicles is called a miniature end plate potential. Spontaneous release of vesicles occurs at a rate of about 1/sec. MEPPs may be important in maintaining the integrity of the muscle fiber. 19. Discuss the end-plate potential (EPP), including its characteristics and underlining mechanisms.Why are its amplitude and duration limited? How does it differ from an action potential? The end-plate potential is the postsynaptic potential produced at push back end plate. The EPP occurs as the result of ACh binding to its receptors on end-plate membrane and opening the chemically gated channels located there. The EPP is a graded potential the magnitude of the EPP is proportional to the number of channels opened by ACh and spreads only passively. The EPP acts as a stimulus for the production of an action potential on the muscle membrane contiguous to the end-plate membrane.The amplitude and duration of the EPP may be limited by the amount of neurotrans mitter released, or by the number of receptors present, or by the normal activity of AChEase. The EPP differs from an action potential in the same shipway that other graded potentials do. 19. How are action potentials initiated at the muscle end plate? What is the ratio of the number of muscle action potentials to motor neuron action potentials (output input)? Action potentials are initiated in the region of the muscle end plate when the membrane is depolarized by the electrotonically spreading EPP.The ratio of the number of muscle action potentials to motor neuron action potentials (output input) is 11. 19. What are chemically gated ion channels? Give an example. How do such channels differ from voltage-gated channels? Chemically-gated ion channels are those channels which open only in response to the binding of a chemical neurotransmitter, hormone or other chemicals and not in response to membrane depolarization as voltage-gated channels do. The channel associated with the ACh re ceptor is a chemically-gated ion channel 26.Compare and contrast the characteristics of chemical and electrical synaptic transmission. Electrical synaptic transmission is mediated by gap junctions. The gap junctions provide a pathway for cytoplasmic continuity. As a result, a depolarization (or hyperpolarization) produced in the presynaptic terminal produces a change in potential in the postsynaptic terminal. There is minimal synaptic delay and the transmission can spread bidirectionally. Electrical junctions are found in the nervous system, as well as smooth muscle and cardiac muscle.Chemical synaptic transmission occurs between two cell membranes separated by a synaptic cleft. The presynaptic terminal contains a high concentration of mitochondria and synaptic vesicles and there is a characteristic thickening of the postsynaptic membrane. Since the neurotransmitter must diffuse across the synaptic cleft and bind to its receptor, there is delay of about 0. 5 1 msec between the init iation of an action potential in the presynaptic terminal and a potential change in the postsynaptic terminal. Chemical transmission is generally unidirectional.