Figure 11–36 a chemical synapse. (A) When an action potential reaches the nerve terminal in a presynaptic cell, it stimulates the terminal to release its neurotransmitter. The neurotransmitter molecules are contained in synaptic vesicles and are released to the cell exterior when the vesicles fuse with the plasma membrane of the nerve terminal. The released neurotransmitter binds to and opens the transmitter-gated ion channels concentrated in the plasma membrane of the postsynaptic target cell at the synapse. The resulting ion flows alter the membrane potential of the postsynaptic membrane, thereby transmitting a signal from the excited nerve (B) (Movie 11.12). (B) A thin-section electron micrograph of two nerve terminal synapses on a dendrite of a postsynaptic cell. (B, courtesy of Cedric Raine.) electrically isolated from one another, the presynaptic cell being separated from the postsynaptic cell by a narrow synaptic cleft. When an action potential arrives at the presynaptic site, the depolarization of the membrane opens voltage-gated Ca2+ channels that are clustered in the presynaptic membrane. Ca2+ influx triggers the release into the cleft of small signal molecules known as neurotransmitters, which are stored in membrane-enclosed synaptic vesicles and released by exocytosis (discussed in Chapter 13). The neurotransmitter diffuses rapidly across the synaptic cleft and provokes an electrical change in the postsynaptic cell by binding to and opening transmitter-gated ion channels (Figure 11–36). After the neurotransmitter has been secreted, it is rapidly removed: it is either destroyed by specific enzymes in the synaptic cleft or taken up by the presynaptic nerve terminal or by surrounding glial cells. Reuptake is mediated by a variety of Na+-dependent neurotransmitter symporters (see Figure 11–8); in this way, neurotransmitters are recycled, allowing cells to keep up with high rates of release. Rapid removal ensures both spatial and temporal precision of signaling at a synapse. It decreases the chances that the neurotransmitter will influence neighboring cells, and it clears the synaptic cleft before the next pulse of neurotransmitter is released, so that the timing of repeated, rapid signaling events can be accurately communicated to the postsynaptic cell. As we shall see, signaling via such chemical synapses is far more versatile and adaptable than direct electrical coupling via gap junctions at electrical synapses (discussed in Chapter 19), which are also used by neurons but to a much smaller extent.
Transmitter-gated ion channels, also called ionotropic receptors, are built for rapidly converting extracellular chemical signals into electrical signals at chemical synapses. The channels are concentrated in a specialized region of the postsynaptic plasma membrane at the synapse and open transiently in response to the binding of neurotransmitter molecules, thereby producing a brief permeability change in the membrane (see Figure 11–36A). Unlike the voltage-gated channels responsible for action potentials, transmitter-gated channels are relatively insensitive to the membrane potential and therefore cannot by themselves produce a self-amplifying excitation. Instead, they produce local permeability increases, and hence changes of membrane potential, that are graded according to the amount of neurotransmitter released at the synapse and how long it persists there. Only if the summation of small depolarizations at this site opens sufficient numbers of nearby voltage-gated cation channels can an action potential be triggered. This may require the opening of transmitter-gated ion channels at numerous synapses in close proximity on the target nerve cell.