Roussel J P, Astier H
Laboratoire de Neurobiologie Endocrinologique, UA 1197 CNRS, Université Montpellier II, France.
Eur J Pharmacol. 1990 Nov 6;190(1-2):135-45. doi: 10.1016/0014-2999(90)94120-m.
The effects of gamma-aminobutyric acid (GABA) and isoguvacine on the thyrotropin (TSH) secretion stimulated by thyrotropin releasing hormone (TRH), were investigated in vitro with perifused rat pituitaries. At nanomolar concentrations the two agonists induced potentiation of the TRH-induced TSH release. The potentiation was blocked by SR 95531 a specific GABAA antagonist. The isoguvacine potentiation of the TSH response to TRH failed to occur when cobalt (Co2+) was added to the perifused medium. Nifedipine completely blocked the GABA or isoguvacine potentiation of the TSH response while omega-conotoxin did not modify it. Pre-perifusion of the pituitaries with pertussis toxin did not change the TSH response to TRH but completely inhibited the isoguvacine potentiation of the response. Our results demonstrate that the GABA potentiation of TRH-induced TSH release occurring through the stimulation of GABAA receptor sites is a calcium (Ca2+)-dependent phenomenon, probably mediated by activation of dihydropyridine (DHP)-sensitive, omega-conotoxin-insensitive Ca2+ channels involving a pertussis toxin-sensitive G protein.
