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This Article Full Text Full Text (PDF) All Versions of this Article: 96/6/3378    most recent 00591.2005v1 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 Google Scholar Google Scholar Articles by Levi, R. Articles by Selverston, A. I. Search for Related Content PubMed PubMed Citation Articles by Levi, R. Articles by Selverston, A. I.

Mechanisms Underlying Type I mGluR-Induced Activation of Lobster Gastric Mill Neurons

Institute for Nonlinear Science, University of California, San Diego, La Jolla, California

Submitted 8 June 2006; accepted in final form 25 August 2006

In addition to ionotropic effects, glutamate and acetylcholine have metabotropic modulatory effects on many neurons. Here we show that in the stomatogastric ganglion of the lobster, glutamate, one of the main ionotropic neurotransmitters, modulates the excitability of gastric mill neurons. The neurons in this well-studied system produce rhythmic output to a subset of lobster foregut muscles. Recently, metabotropic glutamate receptor (mGluR) agonists were suggested as modulators of the rhythmic output, in addition to the previously described muscarinic modulation by acetylcholine. However, the cellular mechanisms responsible for these effects on the pattern are not known. Using intracellular recording methods and calcium imaging, we show that glutamate has an excitatory effect on specific neurons in the stomatogastric ganglion, which is mediated by mGluRs. Responses to the application of mGluR type I agonists are transient oscillations in the system, probably arising from network interactions. We show that the excitatory effect is sensitive to phospholipase-C and IP₃ and is G-protein dependent. The G-protein dependency was demonstrated by GDPS and GTPS injection into identified neurons. The depolarizations and oscillations were accompanied by an increase of intracellular Ca²⁺ levels and correlated Ca²⁺ oscillations. By using cyclopiazonic acid, an endoreticular Ca²⁺ uptake inhibitor, we show that some internal calcium release may augment the response, but is not crucial for its production. Interestingly, although Ca²⁺ concentration increase is typically associated with the phosphoinositide pathway, in the lobster, the Ca²⁺ concentration increase—either voltage dependent or independent—cannot account for the observed depolarization.