Study questions for Action Potential PDF

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Study questions for Chapters on the Action Potential

1) Explain the ionic basis of the action potential. In other words, which ions flow into the cell during the upstroke of the action potential and which flow into the cell during the undershoot or the phase of repolarization? Answer- The upstroke of the action potential is due to the influx of Na ions into the cell causing the membrane potential to approach ENa (the sodium equilibrium potential). The undershoot of the action potential is due to the large efflux of potassium ions causing the cell to approach EK.

2. Explain the general structure of voltage gated sodium and voltage gated potassium channels. What activates each channel and what is the time course of their gate openings? how do they work cooperatively to generate an action potential? Answer- Sodium channels have two gates; a fast acting activation gate that opens quickly when the membrane is depolarized, and a second, inactivation gate, that closes when the cell is depolarized. The inactivation gate closes more slowly than the opening of the activation gate. Therefore, upon depolarization the opening of the activation gate allows for the influx of Na, causing the cell to approach ENa (the sodium equilibrium potential). Potassium channels only have an activation gate that opens with depolarization but more slowly than the activation gate of the sodium channel. The net result is that potassium channel activation gate opens with the closing of sodium inactivation gate. Thus, after the sodium activation gate closes, shutting off any additional sodium influx, the potassium activation gates open, allowing for an efflux of potassium. The large potassium conductance, now unhindered by a sodium conductance, drives the membrane potential to the potassium equilibrium potential (EK) thereby generating the undershoot of the action potential. The high negative membrane potential then resets the activation and inactivation gates on the sodium channels and resets (closes) the activation gate on the potassium channels. 3. What is the definition of threshold for a nerve cell? Explain the competing effects that occur on the sodium and potassium channels upon depolarization of a nerve cell membrane. Answer-Threshold is reached when sodium influx is slightly greater than potassium efflux. The greater sodium influx depolarizes the cell causing even more sodium channels to open resulting in an increasing depolarization. The increasing depolarization then leads to a positive feedback (the rapid opening of more and more sodium channels) resulting in the upstroke of the action potential, where the sodium conductance is so large that the cell approaches the sodium equilibrium potential at the patch of membrane where the channels are open. Since there are some leakage potassium channels open (which produce the resting potential), a small influx of positive charge causes an increased 1

efflux of positive charges carried by potassium. If the efflux of potassium is greater than the influx of sodium, the membrane potential reverts back to its resting state (no action potential is generated). Thus, the open potassium channels at rest act to oppose a small depolarization. 4. What is meant by “inactivation”? What role does inactivation have on the shape of the action potential? Do K+ channels exhibit inactivation? Answer- Inactivation is the slightly delayed closing of sodium channels when the membrane is depolarized. The sequence of events evoked by depolarization is that the activation gates on the sodium channels open quickly, thereby generating the upstroke of the action potential. But a moment later, the inactivation gates close, preventing any further influx of sodium. The inactivation of sodium channels, coupled with the slightly delayed opening of potassium channels, limits the duration of the action potential, making it a short, i.e., ~1.0 millisecond, event. Potassium channels only have an activation gate and do not have an inactivation gate. 5. What are the three main purposes of an action potential that were given in lecture? Answers- To conduct a bit of information, the action potential; a) Over long distances; b) with high fidelity, so that the same action potential that appears at the cell body, appears at the axon terminal a moment later; and c) and the action potential conduction has to be rapid. 6) What would happen along the axon if neurons could not generate action potentials? Answer- the membrane depolarization would decrease along the axon such that there would be no detectable depolarization as short distance from the site of the depolarization. Since the membrane is depolarized for a short distance along the axon, the driving force for potassium would be enhanced at those locations resulting in an efflux of positive charges carried by potassium, and the membrane potential would revert back to the resting potential. 7. What feature(s) of the Na channel is (are) responsible for the refractory period? What important consequence does the refractory period have for the conduction of action potentials? Answer- Two features are critical. First, the inactivation gates on the sodium channels have to be reset (opened). Second, the activation gates have to open. If either of these conditions are not met, the channel cannot open and allow for the influx of sodium to depolarize the membrane. The refractory period limits the rate at which action potentials can be generated.

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8) What effect does the delayed K+ conductance have on the shape of an action potential? What would be the effect on the shape of an action potential if the K+ conductance were blocked? What would be the effect on the shape of the action potential if the K+ conductance only turned on many milliseconds following membrane depolarization? What would be the effect if the K+ conductance turned on at exactly the same time as the Na conductance? Answer- The delayed potassium conductance acts to repolarize the membrane by allowing for the efflux of positive charges (carried by potassium) and thereby make the action potential a very brief event. If the K conductance were blocked, it would take tens of milliseconds for the membrane to repolarize. The repolarization would occur only through the non-voltage gated potassium channels that set the resting potential. If the potassium conductance were delayed by several additional milliseconds, the action potential would have a prolonged shape. If the potassium conductance turned on at exactly the same time as the sodium conductance, the membrane potential would only approach 0.0 millivolts.

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