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: 98/1/43    most recent 00356.2007v1 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 ISI Web of Science 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 Marabese, I. Articles by Maione, S. Search for Related Content PubMed PubMed Citation Articles by Marabese, I. Articles by Maione, S.

Periaqueductal Gray Metabotropic Glutamate Receptor Subtype 7 and 8 Mediate Opposite Effects on Amino Acid Release, Rostral Ventromedial Medulla Cell Activities, and Thermal Nociception

¹Department of Experimental Medicine, Section of Pharmacology "L. Donatelli," Faculty of Medicine and Surgery, Second University of Naples, Naples; ²Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Pozzuoli, Italy; and ³Endocannabinoid Research Group, Institute of Cybernetics "E. Caianiello", Consiglio Nazionale delle Ricerche, Pozzuoli (Naples), Italy

Submitted 29 March 2007; accepted in final form 8 May 2007

The current study has investigated the involvement of periaqueductal gray (PAG) metabotropic glutamate subtype 7 and 8 receptors (mGluR₇ and mGluR₈) in modulating rostral ventromedial medulla (RVM) ongoing and tail flick–related ON and OFF cell activities. Our study has also investigated the role of PAG mGluR₇ on thermoceptive threshold and PAG glutamate and GABA release. Intra-ventrolateral PAG (S)-3,4-dicarboxyphenylglycine [(S)-3,4-DCPG (2 and 4 nmol/rat)] or N,N^I-dibenzhydrylethane-1,2-diamin dihydrochloride (AMN082, (1 and 2 nmol/rat), selective mGluR₈ and mGluR₇ agonists, respectively, caused opposite effects on the ongoing RVM ON and OFF cell activities. Tail flick latency was increased or decreased by (S)-3,4-DCPG or AMN082 (2 nmol/rat), respectively. (S)-3,4-DCPG reduced the pause and delayed the onset of the OFF cell pause. Conversely, AMN082 increased the pause and shortened the onset of OFF cell pause. (S)-3,4-DCPG or AMN082 did not change the tail flick-induced onset of ON-cell peak firing. The tail flick latency and its related electrophysiological effects induced by (S)-3,4-DCPG or AMN082 were prevented by (RS)--methylserine-o-phosphate (100 nmol/rat), a group III mGluR antagonist. Intra-ventrolateral PAG perfusion with AMN082 (10 and 25 µM), decreased thermoceptive thresholds and glutamate extracellular levels. A decrease in GABA release was also observed. These results show that stimulation of PAG mGluR₈ or mGluR₇ could either relieve or worsen pain perception. The opposite effects on pain behavior correlate with the opposite roles played by mGluR₇ and mGluR₈ on glutamate and GABA release and the ongoing and tail flick-related activities of the RVM ON and OFF cells.