The relationship between noradrenergic (NA) stimulatory and γ-aminobutyric acid (GABA)-mediated inhibitory systems in the control of luteinizing hormone (LH) secretion was examined in ovariectomized rats. Stimulation of the GABAA receptor by an intraventricular (i.c.v.) administration of a GABAA agonist, muscimol, significantly attenuated the LH secretory response to the subsequent i.c.v. injection of NA in estrogen-primed rats. On the other hand, blockade of α-adrenergic receptors by phenoxybenzamine did not interfere with the stimulatory effect of an i.c.v. injection of a GABAA antagonist bicuculline. In a different series of experiments, ovariectomized animals had been treated with i.c.v. injections of 6-hydroxydopamine (6-OHDA) or its vehicle. An i.c.v. injection of muscimol or phentolamine significantly inhibited the estrogen-induced surge of LH secretion in vehicle-treated rats. Muscimol also inhibited the existing pulsatile LH secretion in vehicle-treated, estrogen-unprimed animals. In animals in which hypothalamic NA terminals were presumed to be destroyed by 6-OHDA, the inhibitory effect of phentolamine was significantly diminished while that of muscimol was unaltered. These results permit the following conclusions: (1) the central GABAergic system inhibits LH secretion via GABAA receptors; (2) this inhibitory GAB A system operates without mediation by the NA system, and (3) the GABAergic non-NA-mediated system can affect physiological patterns of pituitary LH secretion in female rats.