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Neuromuscular transmission involves the events leading from the liberation of acetylcholine (ACh) at the motor nerve terminal to the generation of end plate currents (EPCs) at the postjunctional site. Release of ACh is initiated by membrane depolarization and influx of Ca++ at the nerve terminal (Fig. 28.1). This leads to a complex process involving docking and fusion of synap-tic vesicles with active sites at the presynaptic membrane. Because ACh is released by exocytosis, functional transmitter release takes place in a quantal fashion. Each quantum corresponds to the contents of one synaptic vesicle (about 10,000 ACh molecules), and about 200 quanta are released with each nerve action potential.

ACh diffusing across the synaptic cleft may bind to ACh receptors (AChRs) to produce an electrical response, interact with acetylcholinesterase (AChE) and be hydrolyzed, or diffuse into the systemic circulation.

AChRs are located primarily at the peaks of the subsyn-aptic folds, whereas AChE is distributed uniformly in the basal lamina at the subsynaptic membrane (Fig. 28.1).

The AChR consists of five subunits surrounding an ion-conducting channel (Fig. 28.2). Activation of the binding sites on the two a-subunits results in a conformational change. This allows the simultaneous inflow of Na+ and Ca++ and outflow of K+, with a net inflow of positive charge. The response to a spontaneously secreted quantum of ACh (that is, activation of several thousand AChRs) is seen as a miniature EPC. With nerve stimulation, many quanta are released synchronously to produce a full-sized EPC, which is the summated response of the 200 or so individual miniature EPCs. The EPC is a local graded current that in normal conditions triggers an action potential in the adjacent muscle membrane (Fig. 28.1).

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