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The effect of N‐ethylmaleimide on transmitter release from the skeletal neuromuscular junction of Bufo marinus
Author(s) -
Knight D.,
Bellingham M.C.,
Lavidis N.A.
Publication year - 2004
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20044
Subject(s) - neuromuscular junction , calcium , neuromuscular transmission , stimulus (psychology) , neurotransmission , biophysics , neural facilitation , chemistry , neuroscience , excitatory postsynaptic potential , biology , endocrinology , biochemistry , inhibitory postsynaptic potential , psychology , receptor , organic chemistry , psychotherapist
N‐ethylmaleimide (NEM) has been used extensively in biochemical assays as an inhibitor of the NEM sensitive fusion protein (NSF). However, examination of the effect of NEM on transmitter release in more physiologically relevant preparations has proved inconclusive. In the present study, we have examined the effect of low concentrations of NEM on synaptic transmission in intact nerve‐muscle preparations from toads ( Bufo marinus ). Under conditions of low transmitter release probability (0.3 mM calcium, 1 mM magnesium), treatment with NEM (10 μM) caused a significant increase in the amplitude of stimulus‐evoked endplate potentials (EPPs) and a significant increase in the frequency of spontaneously occurring miniature EPPS (MEPPS) without affecting the amplitude of MEPPs. When the calcium concentration in the bath was raised to 4 mM, 10 μM NEM had no effect on EPP amplitude. Under these conditions, NEM treatment reduced paired pulse facilitation and increased depression during stimulus trains. Treatment with NEM also resulted in a significant decrease in the synaptic delay. The effects of NEM on transmitter release in the present study were not due to inactivation of G‐proteins. The results of the present study show a calcium‐dependent facilitation of stimulus‐evoked transmitter release by NEM. These results are discussed in terms of the possible sites of NEM action leading to the observed changes in transmitter release. Synapse 53:151–158, 2004. © 2004 Wiley‐Liss, Inc.