Nerve and muscle action potentials occur as a result of sudden changes in permeability of specific ion channels, in response to local perturbations in the voltage of membrane potential. The channels involved are known to be voltage dependent; that is, permeability changes are dependent on changes in membrane potentials. Although voltage-dependent ion channels depend on changes in membrane potential to initiate permeability changes, once those changes occur, they revert back to baseline permeability levels quickly and irrespective of membrane potential. Thus, although an action potential needs a membrane potential change for its initiation, its termination occurs because of processes intrinsic to the channels themselves. Action potentials are, therefore, extremely brief, usually in the order of approx 1 ms. Action potentials are always all-or-none responses, because the voltage-dependent changes discussed either occur completely or not at all. To understand these action potentials, we will discuss what happens during depolarization and repolarization.
The process of action potential generation was first studied in unmyelinated axons of invertebrates. Such axons have both voltage-gated potassium and sodium channels. If a local area of membrane is briefly depolarized (i.e., rendered more positive) by approx 15 mV, a conformational change occurs in both ion channels, such that both become briefly much more permeable. Because of the high concentration of extracellular sodium, as well as the negativity of the intracellular space, sodium will rush into the cell through the open sodium channels. However, after approx 1 ms, the sodium channels revert to their resting, nearly closed, state. The effect of sodium influx is to render the local area of intracellular space
briefly depolarized. In contrast to sodium channels, potassium channels open more slowly and close more slowly. Therefore, relatively long after the sodium channels have reverted to their baseline closed state, potassium channels remain open, allowing positively charged ions to leave and restoring the baseline negativity within the axon. These changes in the sodium and potassium conductance during an action potential are illustrated in Fig. 1. In myelinated axons, however, changes in potassium conductance do not seem to contribute to the repolarization process.
Local changes in myelinated or unmyelinated axons are unimportant in themselves, unless a mechanism exists for them to propagate along the axon. This mechanism is discussed next.
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