Voltage-Gated Ion Channels and the Propagation of Action Potentials in Nerve Cells
■ Action potentials are sudden membrane depolarizations followed by a rapid repolarization. They originate at the axon hillock and move down the axon toward the axon terminals, where the electric impulse is transmitted to other cells via a synapse (see Figures 7-29 and 7-31).
■ An action potential results from the sequential opening and closing of voltage-gated Na+ and K+ channels in the plasma membrane of neurons and muscle cells.
■ Opening of voltage-gated Na+ channels permits influx of Na+ ions for about 1 ms, causing a sudden large depolarization of a segment of the membrane. The channels then close and become unable to open (refractory) for several milliseconds, preventing further Na+ flow (see Figure 7-33).
■ As the action potential reaches its peak, opening of voltage-gated K+ channels permits efflux of K+ ions, which repolarizes and then hyperpolarizes the membrane. As these channels close, the membrane returns to its resting potential (see Figure 7-30).
■ The excess cytosolic cations associated with an action potential generated at one point on an axon spread passively to the adjacent segment, triggering opening of voltage-gated Na+ channels and movement of the action potential along the axon.
■ Because of the absolute refractory period of the voltage-gated Na+ channels and the brief hyperpolarization resulting from K+ efflux, the action potential is propagated in one direction only, toward the axon terminus.
■ Voltage-gated Na+ and Ca2+ channels are monomeric proteins containing four domains that are structurally and functionally similar to each of the subunits in the tetrameric voltage-gated K+ channels.
■ Each domain or subunit in voltage-gated cation channels contains six transmembrane a helices and a nonheli-cal P segment that forms the ion-selectivity pore (see Figure 7-36).
■ Opening of voltage-gated channels results from outward movement of the positively charged S4 a helices in response to a depolarization of sufficient magnitude.
■ Closing and inactivation of voltage-gated cation chan nels result from movement of a cytosolic segment into the open pore (see Figure 7-37).
■ Myelination, which increases the rate of impulse conduction up to a hundredfold, permits the close packing of neurons characteristic of vertebrate brains.
■ In myelinated neurons, voltage-gated Na+ channels are concentrated at the nodes of Ranvier. Depolarization at one node spreads rapidly with little attenuation to the next node, so that the action potential "jumps" from node to node (see Figure 7-40).
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