HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 95/5/3219    most recent 00815.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map 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 HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Hatcher, N. G. Articles by Gillette, R. Search for Related Content PubMed PubMed Citation Articles by Hatcher, N. G. Articles by Gillette, R.

Nitric Oxide Potentiates cAMP-Gated Cation Current in Feeding Neurons of Pleurobranchaea californica Independent of cAMP and cGMP Signaling Pathways

Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois

Submitted 3 August 2005; accepted in final form 1 February 2006

Critical roles for nitric oxide (NO) in regulating cell and tissue physiology are broadly appreciated, but aspects remain to be explored. In the mollusk Pleurobranchaea, NO synthase activity is high in CNS ganglia containing motor networks for feeding and locomotion, where a cAMP-gated cation current (I_Na,cAMP) is also prominent in many neurons. We examined effects of NO on I_Na,cAMP using voltage-clamp methods developed to analyze cAMP signaling in the live neuron, focusing on the identified metacerebral giant neuron of the feeding network. NO donors enhanced the I_Na,cAMP response to injected cAMP by an averaged 85%. In dose-response measures, NO increased the current stimulated by cAMP injection without altering either apparent cAMP binding affinity or cooperativity of current activation. NO did not detectably alter levels of native cAMP or synthesis or degradation rates as observable in both current saturation and decay rate of I_Na,cAMP responses to cAMP injection. NO actions were not exerted by cGMP signaling, as they were not mimicked by cGMP analogue nor blocked by inhibitors of guanylate cyclase and protein kinase G. NO potentiation of I_Na,cAMP was broadly distributed among many other neurons of the feeding motor network in the buccal ganglion. However, NO did not affect a second type of I_Na,cAMP found in locomotor neurons of the pedal ganglia. These results suggest that NO acts through a novel mechanism to regulate the gain of cAMP-dependent neuromodulatory pathways that activate I_Na,cAMP and may thereby affect the set points of feeding network excitability and reactivity to exogenous input.

This article has been cited by other articles:

				V. A. Straub, J. Grant, M. O'Shea, and P. R. Benjamin Modulation of Serotonergic Neurotransmission by Nitric Oxide J Neurophysiol, February 1, 2007; 97(2): 1088 - 1099. [Abstract] [Full Text] [PDF]