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Presynaptic M 2 muscarinic receptors are involved in controlling the kinetics of ACh release at the frog neuromuscular junction
Author(s) -
Slutsky I.,
Silman I.,
Parnas I.,
Parnas H.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.00717.x
Subject(s) - methoctramine , muscarine , neuromuscular junction , excitatory postsynaptic potential , postsynaptic potential , acetylcholine , muscarinic acetylcholine receptor , neuroscience , chemistry , biophysics , depolarization , muscarinic acetylcholine receptor m2 , inhibitory postsynaptic potential , biology , endocrinology , receptor , biochemistry
1 Macropatch recording was used to study release of acetylcholine in the frog neuromuscular junction evoked by either direct local depolarization or by an action potential. 2 The quantal content was established by directly counting the released quanta. The time course of release was obtained by constructing synaptic delay histograms. 3 Perfusion of the neuromuscular junction with methoctramine, a selective M 2 /M 4 muscarinic antagonist, increased the quantal content and slowed the exponential decay of the synaptic delay histograms. Addition of the agonist muscarine reversed these effects. 4 Addition of acetylcholinesterase prolonged the decay of the delay histogram, and muscarine reversed this effect. 5 Methoctramine slowed the rise time of the postsynaptic current produced by axon stimulation without affecting either the excitatory nerve terminal current or the presynaptic Ca 2+ current. 6 These results show that presynaptic M 2 muscarinic receptors are involved in the process which terminates evoked ACh release.