Synopsis
Injections of2mgof progesterone into ovariectomized estrogen-primed rats significantly increased serum LH and FSH concentrations3, 5 and8hr later. Receptor blockers of noradrenaline (NA), dopamine (DA) or acetylcholine (ACH), phenoxybenzamine (20mg/kg body weight), pimozide (1mg/kg body weight) or atropine (700 mg/kg body weight), respectively, prevented the progesterone-induced gonadotropin release. On the other hand, none of them blocked the gonadotropin release following unilateral electrochemical stimulation (100uA for60sec) of the medial preoptic area which occurred0.5and1.5hr later, although pimozide or atropine reduced serum LH concentrations at4.0hr after stimulation. Furthermore, the sites of action of NA, DA and ACH with respect to LH release were examined by intracerebral implantation in ovariectomized estrogen-primed rats. DA or ACH, when implanted unilaterally into the medial preoptic area, induced a significant increase in serum LH5hr later, whereas NA decreased LH levels. Implantations of NA or ACH into the bed nucleus of the stria terminalis or the medial amygdala increased serum LH although the effect of NA into the latter was not statistically significant. Only implantations of NA among the three substances into the lateral septum induced LH release.These results suggest that all of NA, DA and ACH play stimulatory roles in the regulation of gonadotropin secretion, and that there are regional differences of their effectivenesses in releasing L H within the limbic-preoptic area.