Trans-ACPD inhibits cAMP formation via a pertussis toxin-sensitive G-protein.
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.
Manzoni
O
O
Centre CNRS-INSERM de Pharmacologie-Endocrinologie, Montpellier, France.
Prezeau
L
L
Sladeczek
F
F
Bockaert
J
J
D000818:Animals; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D003342:Corpus Striatum / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism*; D003515:Cycloleucine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D019204:GTP-Binding Proteins / Q000378:metabolism*; D037342:Pertussis Toxin; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D010566:Virulence Factors, Bordetella; D003515:Cycloleucine; C036361:1-amino-1,3-dicarboxycyclopentane; D005576:Colforsin; D000242:Cyclic AMP; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins