The Human Brain : From Neurone to Nervous System

NERVE CELLS : THE ACTION POTENTIAL : Ionic Movements


  1. During the action potential there are rapid transient changes in the transmembrane potential: at its peak the membrane potential reaches nearly +40 mV (approaching the equilibrium potential for sodium), then rapidly declines to below the previously existing resting potential (a phase known as the afterpotential) before slowly returning to normal.

  2. Action potentials are initiated by depolarisation of the resting membrane to a threshold membrane potential of about -55 mV, at which point voltage-gated sodium channels open and allow sodium ions to enter the axoplasm.

  3. The repolarisation phase of the action potential is due to the inactivation and closure of voltage gated sodium channels and the opening of voltage-gated potassium channels, which are also responsible for the afterpotential.

  4. The voltage-gated sodium channel behaves as though it has two gates:
    • the first opens on depolarisation to around -55mV
    • the second stops inward movement of sodium ions by closing the channel at a different site within the protein pore as soon as the depolarisation has occurred - the latter is know as the inactivation gate.

  5. During the depolarisation phase of the action potential (the 'spike'), some sodium ions enter the axon when the voltage-gated sodium channel opens and cease when the gate is inactivated. During this period the axon in inexcitable (during the absolute refractory period)

  6. Once the depolararisation phase has occurred, voltage gated sodium channels become inactivated and voltage gated potassium channels begin to open.

  7. The opening and closure of voltage-gated potassium channels following the spike are essential for repolarisation (and for the afterpotential, during which the axon is less excitable than normal (the relative refractory period).

  8. Voltage gated sodium channels (also called Nav channels) are composed of proteins that change their shape to allow sodium ions to move when the voltage gate opens and before the inactivation gate closes. Mutations of these proteins allow different rates of sodium entry, and for different periods.

  9. One mutation is associated with certain chronic pain states, because the action potential is prolonged, resulting in increased transmitter release at synapses the pain pathway.
Key Words: Action potential, 'Spike', voltage gated sodium channels, the inactivation gate; voltage gated potassium channels, Nav channels.







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