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J. Biol. Chem., Vol. 277, Issue 2, 1223-1228, January 11, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/2/1223    most recent M109141200v1 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 Google Scholar Google Scholar Articles by Perroy, J. Articles by Fagni, L. Search for Related Content PubMed PubMed Citation Articles by Perroy, J. Articles by Fagni, L. Social Bookmarking                      What's this?

Permissive Effect of Voltage on mGlu 7 Receptor Subtype Signaling in Neurons^*

Julie Perroy, Sylvain Richard, Joel Nargeot, Joel Bockaert, and Laurent Fagni^§

From the CNRS-UPR 9023 CCIPE and  CNRS-UPR 1142 IGH, 141 Rue de la Cardonille, 34094 Montpellier, Cedex 05, France

G protein-coupled receptors mobilize neuronal signaling cascades which until now have not been shown to depend on the state of membrane depolarization. Thus we have previously shown that the metabotropic glutamate receptor type 7 (mGlu7 receptor) blocks P/Q-type Ca²⁺ channels via activation of a G_o protein and PKC, in cerebellar granule cells. We show here that the transient depolarizations used to evoke the studied Ca²⁺ current were indeed permissive to activate this pathway by a mGlu7 receptor agonist. Indeed, sustained depolarization to 0 mV was sufficient to inhibit P/Q-type Ca²⁺ channels. This effect involved a conformational change in voltage-gated sodium channel independently of Na⁺ flux, activation of a pertussis toxin-sensitive G-protein, inositol trisphosphate formation, intracellular Ca²⁺ release, and PKC activity. Subliminal sustained membrane depolarization became efficient in inducing inositol trisphosphate formation, release of intracellular Ca²⁺ and in blocking Ca²⁺ channels, when applied concomitantly with the mGlu7a receptor agonist, D,L-aminophosphonobutyrate. This synergistic effect of membrane depolarization and mGlu7 receptor activation provides a mechanism by which neuronal excitation could control action of the mGlu7 receptor in neurons.

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