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Presynaptic effects of muscarine on ACh release at the frog neuromuscular junction
Author(s) -
Slutsky I.,
Parnas H.,
Parnas I.
Publication year - 1999
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.1469-7793.1999.769ad.x
Subject(s) - muscarine , methoctramine , depolarization , chemistry , acetylcholine , inhibitory postsynaptic potential , neuromuscular junction , muscarinic acetylcholine receptor , biophysics , pirenzepine , endocrinology , neuroscience , receptor , biology , biochemistry
1 Presynaptic effects of muscarine on neurotransmitter release were studied at the frog neuromuscular junction, using focal depolarization of the presynaptic terminal to different levels. 2 Muscarine (10 μM) had a dual effect on ACh release: concomitant inhibition and enhancement of release at the same patch of presynaptic membrane. 3 These two effects were maximal at low depolarizing pulses and diminished as depolarization increased. 4 At low depolarizing pulses, atropine (1 μM) enhanced release, suggesting that ACh in the synaptic cleft causes a net tonic inhibition of ACh release. 5 In the presence of the M 2 antagonist methoctramine (1 μM), muscarine (10 μM) enhanced ACh release. 6 In the presence of the M 1 antagonist pirenzepine (10 μM), muscarine (10 μM) produced stronger inhibition. 7 These results show that the M 2 receptor is responsible for inhibition of ACh release, while the M 1 receptor is responsible for its enhancement. 8 The inhibitory effect of muscarine did not depend on extracellular [Ca 2+ ]. Enhancement of release was abolished at low extracellular [Ca 2+ ]. 9 The muscarine inhibitory effect was not associated with a reduction of Ca 2+ current, while release enhancement was associated with an increase of Ca 2+ current.