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Nitric oxide, cAMP and the biphasic muscarinic modulation of ACh release at the lizard neuromuscular junction
Author(s) -
Graves Austin R.,
Lewin Katherine A.,
A. Lindgren Clark
Publication year - 2004
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 - 10.1113/jphysiol.2004.064469
Subject(s) - muscarine , muscarinic acetylcholine receptor , acetylcholine , neuromuscular junction , nitric oxide , muscarinic acetylcholine receptor m4 , cholinergic , chemistry , muscarinic acetylcholine receptor m2 , acetylcholine receptor , receptor , muscarinic acetylcholine receptor m3 , neuroscience , microbiology and biotechnology , biology , endocrinology , biochemistry
In this study, we characterized the pharmacology and physiology of the automodulation of ACh release at the lizard neuromuscular junction (NMJ). The activation of muscarinic ACh receptors generated a biphasic modulation of synaptic transmission. Muscarine‐induced activation of M 3 receptors (0–12 min) decreased release, whereas M 1 activation (> 12 min) enhanced release. Both phases of the biphasic effect are dependent on nitric oxide. However, cAMP acting via protein kinase A is also necessary for the M 1 effect. In summary, we present a novel biphasic role for muscarine and implicate M 3 receptors in the inhibition and M 1 receptors in the enhancement of transmitter releaseat the cholinergic lizard NMJ.