Abstract

To a certain degree, the events underlying the action potential are understood. For each ion to which the membrane is permeable, there exists an equilibrium potential, whose physical origin is in the activity gradient for that ion. The membrane potential is then the summation of these individual ionic batteries each weighted according to the membrane permeability to that ion. In nerve fibres at rest the potassium permeability is relatively high and the membrane potential is near to the equilibrium potential for potassium. During excitation there is a transitory increase in the permeability to sodium and a slower transitory increase in the potassium permeability also. The membrane potential, therefore, temporarily moves to a value near to the sodium equilibrium potential and then returns to its resting value. Less well understood are the molecular mechanisms responsible for these selective changes in membrane permeability, i.e. how it is that a channel (pathway bywhich an ion traverses the membrane) changes its availability for ion passage as a response to a change in the membrane potential. This is the gating process.

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