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PMID: 1323480 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Trans-ACPD inhibits cAMP formation via a pertussis toxin-sensitive G-protein.

European journal of pharmacology ·Vol. 225 ·No. 4 ·1992-04-10 ·Pages 357-8

Manzoni O, Prezeau L, Sladeczek F, Bockaert J

Abstract

In primary cultured striatal neurons we found that (+-)-trans-1-amino-cyclopentyl-1,3-dicarboxylate (trans-ACPD) could inhibit forskolin-induced cAMP formation in a dose-dependent manner (EC50 156 +/- 38 microM, n = 5, maximal inhibition 37.8 +/- 1.2, n = 37). The trans-ACPD-induced inhibition was totally abolished in neurons preincubated with Bordetella pertussis toxin (1 microgram/ml), demonstrating the involvement of a G-protein. This is the first report in intact neurons of a glutamate metabotropic receptor negatively coupled to cAMP formation.

MeSH Terms
Animals Cells, Cultured Colforsin/pharmacology Corpus Striatum/cytology,drug effects,metabolism Cyclic AMP/metabolism Cycloleucine/analogs & derivatives,pharmacology Dose-Response Relationship, Drug GTP-Binding Proteins/metabolism Pertussis Toxin Virulence Factors, Bordetella/pharmacology
Chemicals
Virulence Factors, Bordetella Cycloleucine 1-amino-1,3-dicarboxycyclopentane Colforsin Cyclic AMP Pertussis Toxin GTP-Binding Proteins
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Manzoni O
Centre CNRS-INSERM de Pharmacologie-Endocrinologie, Montpellier, France.
Prezeau L
Sladeczek F
Bockaert J
Article Info
Journal
European journal of pharmacology
Abbr.
Eur J Pharmacol
ISSN
0014-2999
Published
1992-04-10
Pages
357-8
Language
English
Region
Netherlands
NLM ID
1254354
Subset
IM
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