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First published online on July 2, 2004.
 Copyright © 2004 by The Physiological Society
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jphysiol.2004.064469v1
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Received March 16, 2004
Revised April 13, 2004
Accepted after revision June 30, 2004

Nitric Oxide, cAMP and the Biphasic Muscarinic Modulation of ACh Release at the Lizard Neuromuscular Junction

Austin R Graves1, Katherine A Lewin1, and Clark A Lindgren1*

1 Grinnell College

* To whom correspondence should be addressed. E-mail: lindgren{at}grinnell.edu.

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 M3 receptors (0-12 min) decreased release, whereas M1 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 M1 effect. In summary, we present a novel biphasic role for muscarine and implicate M3 receptors in the inhibition and M1receptors in the enhancement of transmitter release at the cholinergic lizard nmj.


Key words: Muscarinic response • Neuromuscular junction • Nitric oxide






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