GABAERGIC REGULATION OF TUBEROINFUNDIBULAR DOPAMINERGIC-NEURONS IN THE MALE-RAT

The purpose of the present study was to examine the effects of gamma-aminobutyric acid (GABA)(A) and GABA(B) receptor blockade and activation on the activity of tuberoinfundibular dopaminergic (TIDA) neurons in male rats. The activity of TIDA neurons was estimated by measuring the concentration of the primary dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence. Administration of the GABA(A) receptor antagonist SR 95531 increased DOPAC concentrations in the median eminence, and decreased plasma concentrations of prolactin, in a dose- and time-related manner. Administration of the GABA(A) receptor agonist isoguvacine had no effect per se on DOPAC concentrations in the median eminence, but produced a delayed decrease in plasma prolactin concentrations. Isoguvacine pre-treatment prevented the increase in DOPAC concentrations in the median eminence produced by SR 95531. In contrast, administration of the GABA(B) receptor agonist baclofen decreased DOPAC concentrations in the median eminence, and increased plasma prolactin concentrations in a dose-dependent manner. Administration of the GABA(B) receptor antagonist 2-hydroxysaclofen had no effect on TIDA neurons per se, but blocked baclofen-induced decreases in DOPAC concentrations in the median eminence and increases in plasma prolactin concentrations. These results indicate that while activation of GABA(B) receptors inhibits TIDA neurons, these neurons are tonically inhibited by endogenous GABA acting at GABA(A) but not GABA(B) receptors.