Gaba augments basal and electrically stimulated H-3-norepinephrine release in hypothalamic, preoptic area and cortical slices of female rats

These studies examined the regulation by GABA of norepinephrine release from hypothalamus, preoptic area and frontal cortex. Using superfused brain slices from female rats, we show that 100 mu M GABA enhances both basal and electrically stimulated release of H-3-norepinephrine in all three brain regions. The GABA(A) agonist muscimol (100 mu M) significantly augments H-3-norepinephrine release, but it is somewhat less effective than GABA. The GABA, agonist baclofen has little or no effect on basal H-3-norepinephrine efflux. GABA also augments both the magnitude and duration of electrically evoked H-3-norepinephrine release in slices from all three brain regions. GABA facilitation of electrically stimulated H-3-norepinephrine release is mediated through GABA(A) receptors as evidenced by its blockade by 10 mu M bicuculline, a GABA(A) anatgonist, but not by 200 mu M 2-OH saclofen, a GABA(B) antagonist. These data show that the inhibitory amino acid neurotransmitter GABA enhances both basal and evoked release of H-3-norepinephrine in brain slices from female rats. These effects are predominantly mediated by GABA(A) receptors. GABA modulation of hypothalamic norepinephrine release may play a role in the regulation of gonadotropin secretion and reproductive behaviors such as lordosis. (C) 1997 Elsevier Science Ltd. All rights reserved.