Up to this point we have tried to explain how the membrane potential is maintained. This balance changes, however, when the cell is depolarized sufficiently to trigger an action potential. A transient depolarizing potential, such as an excitatory synaptic potential, causes some voltage- gated Na channels to open,and the resultant increase in membrane Na permeability allows Na influx to overpass the K efflux. Thus a net influx of positive charge flows through the membrane, and positive charges accumulate inside the cell, causing further depolarization.

The increase in depolarization causes more voltage gated Na channels to open, resulting in a greater influx of positive charge, which accelerates the depolarization still further.

This positive feedback cycle, develops exponentially driving the membrane potential toward the positive values. On the other hand, K efflux continues through the K channels, and a slight diffusion of Cl into the cell also counteracts the depolarizing tendency of the Na influx. Nevertheless so many voltage-gated Na channels open during the rising phase of the action potential that the permeability to Na is much greater than that of Cl and K. There are two processes that repolarize the membrane, terminating the action potential. First , as the depolarization continues, it slowly turns off, or inactivates, the voltage gated Na channels. This is so, because Na channels have tow types of gating mechanisms: activation, which rapidly opens that channel in response to depolarization, and inactivation which closes the channel if the depolarization is maintained.

The second repolarization process results from the delayed opening of voltage gated K channels. As K channels begin to open, K efflux increases. The delayed increase in K efflux combined with a decrease in Na influx to produce a net efflux of positive charge from the cell, which continues until the cell has repolarized to its resting value.

Note that this process results in a wave of depolarization/repolarization that can propagate all over the surface of the cell's axon (which is the cell structure actually devoted to the generation of the action potential). Once the depolarization/repolarization wave reaches the axon terminal it turns on the mechanisms of synaptic transmission which results in the necessary communication between nerve cells.

Thus the action potential is used by the nerve cell as a propagating signal. The most common site of initiation of the action potential is the axon hillock where the highest concentration of voltage gated ion channels is found.

The whole picture of electric signaling can be summarized as follows:

I.-The interaction of a neurotransmitter (or , alternatively, the activation of a sensory receptor system) with receptor molecules on the external membranes of the neuron (which occur mainly on the dendritic tree or the cell soma), initiates a synaptic potential. The synaptic potential spreads passively (there are no voltage gated ion channels involved in this process) to the axon hillock or initial segments of the axon.

II.- At the trigger zone, the synaptic potential may or may not (depending on whether the actual amplitude of the arriving potential exceeds the threshold of the voltage gated channels) initiate an action potential that propagates actively to the terminal of the neuron.

III.- Finally, at the terminal, the action potential causes transmitter release, which triggers a synaptic potential in the target cell.

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