JN Miami Valley Hospital
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


J Neurophysiol (August 30, 2006). doi:10.1152/jn.00591.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
96/6/3378    most recent
00591.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Levi, R.
Right arrow Articles by Selverston, A. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Levi, R.
Right arrow Articles by Selverston, A. I.
Submitted on June 7, 2005
Accepted on August 25, 2006

Mechanisms underlying type I mGluR-induced activation of lobster gastric mill neurons

Rafael Levi1* and Allen I. Selverston1

1 Institute for Nonlinear science, University of California, San Diego, La Jolla, California, United States

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

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 STG, which is mediated by mGluRs. The response to mGluR type I agonists application is transient oscillations in the system, probably due to network interactions. We show that the excitatory effect is phospholipase-C and IP3 sensitive, as well as, G-protein dependent. The G-protein dependence was demonstrated by GDP{beta}S and GTP{gamma}S injection into identified neurons. The depolarization and oscillation were accompanied by an increase of intracellular Ca2+ levels and correlated Ca2+ oscillations. By using cyclopiazonic acid, an ER 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, Ca2+ concentration increase, either voltage dependent or independent, cannot account for the observed depolarization.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2006 by the The American Physiological Society.