Differential effects of GABAA and GABAB receptor agonists on NMDA-induced and noradrenaline-induced luteinizing-hormone release in the ovariectomized estrogen-primed rat.

Effects of selective gamma-aminobutyric acidA (GABAA) and GABAB receptor agonists on noradrenaline (NA)-induced and N-methyl-D-aspartate (NMDA)-induced luteinizing-hormone (LH) secretion were examined in ovariectomized estrogen-primed rats. Experiments were performed in unanesthetized animals bearing chronic intracerebroventricular (i.c.v.) cannulae. I.c.v. injections of NA or NMDA stimulated LH secretion in animals that had received prior i.c.v. injections of saline. The effects of NA and NMDA were significantly attenuated by a prior i.c.v. injection of phentolamine (a selective alpha-adrenergic-receptor blocker) and 2-amino-5-phosphonovaleric acid (a selective NMDA receptor antagonist), respectively. NA-induced LH release was also inhibited by i.c.v. injections of either muscimol (a selective GABAA receptor agonist) or baclofen (a selective GABAB receptor agonist). On the other hand, although muscimol inhibited the effect of NMDA, baclofen did not inhibit but slightly augmented the NMDA-induced release of LH. These results support the hypothesis that both GABAA and GABAB receptors are involved in the GABAergic inhibition of LH secretion, and further suggest that they are probably located at different sites in the neural mechanism regulating LH secretion in the female rat.