2.1.4: The Change in Membrane Potential During an Action Potential

We discussed previously which ions are involved in maintaining the resting membrane potential. Not surprisingly, some of these same ions are involved in the action potential. When the cell becomes depolarized (more positively charged) and reaches the threshold of excitation, this causes a voltage-dependent Na+ channel to open. A voltage-dependent ion channel is a channel that opens, allowing some ions to enter or exit the cell, depending upon when the cell reaches a particular membrane potential. When the cell is at resting membrane potential, these voltage-dependent Na+ channels are closed. As we learned earlier, both diffusion and electrostatic pressure are pushing Na+ inside the cells. However, Na+ cannot permeate the membrane when the cell is at rest. Now that these channels are open, Na+ rushes inside the cell, causing the cell to become very positively charged relative to the outside of the cell. This is responsible for the rising or depolarizing phase of the action potential (see Figure 5). The inside of the cell becomes very positively charged, +40mV. At this point, the Na+ channels close and become refractory. This means the Na+ channels cannot reopen again until after the cell returns to the resting membrane potential. Thus, a new action potential cannot occur during the refractory period. The refractory period also ensures the action potential can only move in one direction down the axon, away from the soma. As the cell becomes more depolarized, a second type of voltage-dependent channel opens; this channel is permeable to K+. With the cell very positive relative to the outside of the cell (depolarized) and the high concentration of K+ within the cell, both the force of diffusion and the force of electrostatic pressure drive K+ outside of the cell. The movement of K+ out of the cell causes the cell potential to return back to the resting membrane potential, the falling or hyperpolarizing phase of the action potential (see Figure 5). A short hyperpolarization occurs partially due to the gradual closing of the K+ channels. With the Na+ closed, electrostatic pressure continues to push K+ out of the cell. In addition, the sodium-potassium pump is pushing Na+ out of the cell. The cell returns to the resting membrane potential, and the excess extracellular K+ diffuses away. This exchange of Na+ and K+ ions happens very rapidly, in less than 1 msec. The action potential occurs in a wave-like motion down the axon until it reaches the terminal button. Only the ion channels in very close proximity to the action potential are affected.

Figure 6. Summary of the electrochemical communication within and between neurons.

Earlier you learned that axons are covered in myelin. Let us consider how myelin speeds up the process of the action potential. There are gaps in the myelin sheaths called nodes of Ranvier. The myelin insulates the axon and does not allow any fluid to exist between the myelin and cell membrane. Under the myelin, when the Na+ and K+ channels open, no ions flow between the intracellular and extracellular fluid. This saves the cell from having to expend the energy necessary to rectify or regain the resting membrane potential. (Remember, the pumps need ATP to run.) Under the myelin, the action potential degrades some, but is still large enough in potential to trigger a new action potential at the next node of Ranvier. Thus, the action potential actively jumps from node to node; this process is known as saltatory conduction.

In the presynaptic terminal button, the action potential triggers the release of neurotransmitters (see Figure 3). Neurotransmitters cross the synaptic gap and open subtypes of receptors in a lock-and-key fashion (see Figure 3). Depending on the type of neurotransmitter, an EPSP or IPSP occurs in the dendrite of the post-synaptic cell. Neurotransmitters that open Na+ or calcium (Ca+) channels cause an EPSP; an example is the NMDA receptors, which are activated by glutamate (the main excitatory neurotransmitter in the brain). In contrast, neurotransmitters that open Cl- or K+ channels cause an IPSP; an example is gamma-aminobutryric acid (GABA) receptors, which are activated by GABA, the main inhibitory neurotransmitter in the brain. Once the EPSPs and IPSPs occur in the postsynaptic site, the process of communication within and between neurons cycles on (see Figure 6). A neurotransmitter that does not bind to receptors is broken down and inactivated by enzymes or glial cells, or it is taken back into the presynaptic terminal button in a process called reuptake, which will be discussed further in the module on psychopharmacology.

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