Presynaptic Action Potential and Acetylcholine Release

The trigger for ACh release is an action potential in the synaptic terminal. The key aspect of the action potential is that it depolarizes the synaptic terminal,

Figure 8-1 The sequence of events during transmission at a chemical synapse.

Figure 8-2 The chemical structure of acetylcholine (ACh), the chemical neurotransmitter at the neuromuscular junction.

and any stimulus that depolarizes the synaptic terminal causes ACh to be released. The coupling between depolarization and release is not direct, however. The signal that mediates this coupling is the influx into the synaptic terminal of an ion in the ECF that we have largely ignored to this point calcium ions.

Calcium is present at a low concentration in the ECF (1-2 mM) and is not important in resting membrane potentials or in most nerve action potentials, although some action potentials have a contribution from calcium influx (see Chapter 6). However, calcium ions must be present in the ECF in order for release of chemical neurotransmitter to occur. If calcium ions are removed from the ECF, depolarization of the synaptic terminal can no longer induce release of ACh. Depolarization causes external calcium ions to enter the synaptic terminal, and the calcium in turn causes ACh to be released from the terminal.

What mechanism provides the link between depolarization of the terminal and influx of calcium ions? As we've seen in earlier chapters, ions cross membranes through specialized transmembrane channels, and calcium ions are no different in this regard. The membrane of the synaptic terminal contains calcium channels that are closed as long as Em is near its normal resting level. These channels are similar in behavior to the voltage-dependent potassium

1. Presynaptic action potential

2. Depolarization of synaptic terminal

3. Release of chemical neurotransmitter molecules 1

4. Neurotransmitter molecules bind to special receptors on postsynaptic cell

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