Nitric oxide, cAMP and the biphasic muscarinic modulation of ACh release at the lizard neuromuscular junction | Zendy

Graves Austin R. | Zendy; Lewin Katherine A. | Zendy; A. Lindgren Clark | Zendy

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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.

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