Abstract
An action potential is a transient reversal of the membrane potential that occurs in excitable cells, including neurons, muscle cells and some endocrine cells. The action potential is an ‘all-or-nothing’ event: if the triggering stimulus is smaller than a threshold value, the action potential does not occur. But once triggered, the action potential has a well-defined amplitude and duration. Action potential propagation allows rapid signalling within excitable cells over relatively long distances.
What is an action potential?
An action potential is a transient reversal of the membrane potential that occurs in excitable cells, including neurons, muscle cells and some endocrine cells. The action potential is an ‘all-or-nothing’ event: if the triggering stimulus is smaller than a threshold value, the action potential does not occur. But once triggered, the action potential has a well-defined amplitude and duration. Action potential propagation allows rapid signalling within excitable cells over relatively long distances.
Describe the events that result in the nerve action potential
Action potentials usually begin at the axon hillock of motor neurons or at sensory receptors in sensory afferent neurons. Events proceed as follows (Figure 52.1a):
As discussed in Chapter 51, the neuronal resting membrane potential (RMP) of approximately –70 mV is relatively close to the Nernst equilibrium potential for K+ of around –90 mV.
An initial depolarisation of a sensory receptor, synapse or another part of the nerve results in Na+ and K+ movements, producing a net depolarisation of the cell membrane:
– If the stimulus is small, the Na+ influx is exceeded by K+ efflux through K+ leak channels primarily responsible for the RMP (see Chapter 51). The cell membrane returns to –70 mV.
– If the stimulus is large enough, depolarising the cell membrane to approximately –55 mV1 results in a significant activation of transmembrane voltage-gated Na+ channels; Na+ influx then exceeds K+ efflux. This is known as the ‘threshold potential’.
The resulting membrane depolarisation leads to further opening of voltage-gated Na+ channels, thus further increasing the membrane permeability to Na+ (Figure 52.1b). This further increases the Na+ influx, which in turn produces further membrane depolarisation, resulting in the rapid upstroke of the action potential. This drives the membrane potential towards the Nernst equilibrium potential for Na+ of approximately +50 mV. However, the action potential never reaches this theoretical maximum, as two further events intervene:
– Inactivation of voltage-gated Na+ channels: the voltage-gated Na+ channels make a further transition from the open state to an inactivated (refractory) state; membrane Na+ permeability decreases.
– Delayed activation of voltage-gated K+ channels: membrane depolarisation slowly opens voltage-gated K+ channels (Figure 52.1b). Membrane K+ permeability increases and the resulting K+ efflux acts to drive the membrane potential back towards the Nernst equilibrium potential for K+ of approximately –90 mV.
The membrane potential briefly becomes more negative than the RMP. This after-hyperpolarisation occurs because of the gradual closure of the voltage-gated K+ channels, which results in the membrane being briefly more permeable to K+ than at the RMP, thus achieving a value closer to the EK.
In summary, the action potential results from a brief increase in membrane conductance to Na+ followed by a slower increase in membrane conductance to K+ (Figure 52.1b).
How are action potentials propagated along nerve axons?
Electrical depolarisation propagates by the formation of local circuits (Figure 52.2):
The intracellular surface of a resting portion of cell membrane is negatively charged.
Following an action potential, a portion of cell membrane depolarises, resulting in the intracellular surface becoming positively charged. The action potential is limited to a small portion of cell membrane; neighbouring segments remain quiescent.
Ion movement at the edges of the depolarised cell membrane results in current flow; the neighbouring quiescent portions of cell membrane become depolarised.
Current decays exponentially along the length of the nerve axon with a length constant of a few millimetres.2 Nevertheless, provided the propagated depolarisation in the previously quiescent cell membrane is sufficient to reach threshold potential, an action potential is generated.
This process of local circuit propagation and action potential generation is continued until the action potential reaches its destination (Figure 52.2).
