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

Eur J Pharmacol. 1992 Apr 10;225(4):357-8. doi: 10.1016/0922-4106(92)90112-9.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Colforsin / pharmacology
  • Corpus Striatum / cytology
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism*
  • Cyclic AMP / metabolism*
  • Cycloleucine / analogs & derivatives*
  • Cycloleucine / pharmacology
  • Dose-Response Relationship, Drug
  • GTP-Binding Proteins / metabolism*
  • Pertussis Toxin
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Virulence Factors, Bordetella
  • Cycloleucine
  • 1-amino-1,3-dicarboxycyclopentane
  • Colforsin
  • Cyclic AMP
  • Pertussis Toxin
  • GTP-Binding Proteins