The membrane of an axon has many voltage-gated ion channels, most of which open when the membrane potential crosses a threshold value of around -50 mV. When this occurs at the trigger zone, voltage-gated sodium channels rapidly open, causing sodium to enter and depolarize the membrane. This causes an explosive chain reaction by triggering voltage-gated sodium channels in nearby membrane to rapidly open, which repeats until all of these channels open in a wave that rapidly spreads down the axon. The trigger zone has the greatest density of voltage-gated sodium channels, which is why action potentials usually start there. So many sodium channels open that the membrane permeability to sodium is greatly increased, causing the membrane potential to rapidly move toward the equilibrium potential of sodium, which is around +50 mV. This is called the rising phase of the action potential. The action potential usually peaks around +40 mV instead of reaching the sodium equilibrium potential, however, because the voltage-gated sodium channels start automatically closing from higher potential values during the rising phase, after which they are inactivated and unable to open at any membrane potential for a brief time.

While this is happening, but mostly after the large entry of sodium, potassium starts to rapidly exit the neuron. Potassium exits the neuron at this time through two types of channels. The first are the leak channels responsible for the resting potential. During the action potential more potassium exits the neuron through the leak channels because the electrical force driving potassium out of the neuron is greater during the brief time that the inside of the neuron membrane is positively charged. The second are voltage-gated potassium channels in the axon membrane that also open over the threshold potential, but which tend to open slower than the voltage-gated sodium channels. So many potassium channels open that the membrane permeability to potassium is greatly increased, causing the membrane potential to rapidly move toward the equilibrium potential of potassium of around -70 mV. This is called the falling phase of the action potential. This wave of negative membrane potential follows directly on the heels of the wave of positive membrane potential as they both move rapidly along the axon.

The membrane permeability to potassium gradually returns to the resting amount as the voltage-gated potassium channels gradually close from the low potential values, which they tend to do more slowly than the voltage-gated sodium channels. As these channels close the membrane potential returns to the resting potential of around -60 mV. The period of hyperpolarization prior to return to the resting potential is called the afterhyperpolarization. It is also called the refractory period because during this time it is difficult or impossible to trigger an action potential. The first part is called the absolute refractory period because the inactivated voltage-gated sodium channels are unable to open at any membrane potential. The second part is called the relative refractory period because the voltage-gated sodium channels are functional again, but the membrane is hyperpolarized, so that more excitatory input than normal is required to reach the threshold potential. One important effect of the refractory period is that action potentials only travel from the trigger zone to the axon terminals, and they do not turn around and go backward. The features of action potentials vary between neurons, because different types of neurons have different types of voltage-gated ion channels.

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Level 3 Unit 1 Part 15: Effects of axon diameter and myelination