Abstract
Voltage-gated sodium channels subserve regenerative excitation throughout the nervous system, as well as in skeletal and cardiac muscle. This excitation results from a voltage-dependent mechanism that increases regeneratively and selectively the sodium conductance of the channel e-fold for a 4–7 mV depolarization of the membrane with time constants in the range of tens of microseconds. Entry of Na+ into the cell without a companion anion depolarizes the cell. This depolarization, called the action potential, is propagated at rates of 1–20 meters/sec. In nerve it subserves rapid transmission of information and, in muscle cells, coordinates the trigger for contraction. Sodium-dependent action potentials depolarize the membrane to inside positive values of about 30–40 mV (approaching the electrochemical potential for the transmembrane sodium gradient). Repolarization to the resting potential (usually between –60 and –90 mV) occurs because of inactivation (closure) of sodium channels, which is assisted in different tissues by variable amounts of activation of voltage-gated potassium channels. This sequence results in all-or-nothing action potentials in nerve and fast skeletal muscle of 1–2 ms duration, and in heart muscle of 100–300 ms duration. Recovery of regenerative excitation, i.e., recovery of the ability of sodium channels to open, occurs after restoration of the resting potential with time constants of a few to several hundreds of milliseconds, depending on the channel isoform, and this rate controls the minimum interval for repetitive action potentials (refractory period).
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Hanck, D.A., Fozzard, H.A. (2007). Voltage-Gated Sodium Channels. In: Chung, SH., Andersen, O.S., Krishnamurthy, V. (eds) Biological Membrane Ion Channels. Biological And Medical Physics Biomedical Engineering. Springer, New York, NY. https://doi.org/10.1007/0-387-68919-2_6
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