Presynaptic M2 muscarinic receptors are involved in controlling the kinetics of ACh release at the frog neuromuscular junction
- 1Macropatch recording was used to study release of acetylcholine in the frog neuromuscular junction evoked by either direct local depolarization or by an action potential.
- 2The quantal content was established by directly counting the released quanta. The time course of release was obtained by constructing synaptic delay histograms.
- 3Perfusion of the neuromuscular junction with methoctramine, a selective M2/M4 muscarinic antagonist, increased the quantal content and slowed the exponential decay of the synaptic delay histograms. Addition of the agonist muscarine reversed these effects.
- 4Addition of acetylcholinesterase prolonged the decay of the delay histogram, and muscarine reversed this effect.
- 5Methoctramine slowed the rise time of the postsynaptic current produced by axon stimulation without affecting either the excitatory nerve terminal current or the presynaptic Ca2+ current.
- 6These results show that presynaptic M2 muscarinic receptors are involved in the process which terminates evoked ACh release.