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This Article Full Text Full Text (PDF) All Versions of this Article: 559/2/423    most recent jphysiol.2004.064469v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Graves, A. R. Articles by A. Lindgren, C. Search for Related Content PubMed PubMed Citation Articles by Graves, A. R. Articles by A. Lindgren, C.

Department of Biology, Grinnell College, Grinnell, IA 50112, USA

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 M₁ receptors in the enhancement of transmitter releaseat the cholinergic lizard NMJ.

(Received 16 March 2004; accepted after revision 30 June 2004; first published online 2 July 2004)
Corresponding author C. A. Lindgren: Department of Biology Grinnell College 1116 8th Avenue Grinnell, IA 50112, USA. Email: lindgren{at}grinnell.edu