The stimulatory roles of catecholamines and acetylcholine in the regulation of gonadotropin release in ovariectomized estrogen-primed rats.

Abstract

Injections of 2 mg of progesterone into ovariectomized estrogen-primed rats significantly increased serum LH and FSH concentrations 3, 5 and 8 hr later. Receptor blockers of noradrenaline (NA), dopamine (DA) or acetylcholine (ACH), phenoxybenzamine (20 mg/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 (100 microA for 60 sec) of the medial preoptic area which occurred 0.5 and 1.5 hr later, although pimozide or atropine reduced serum LH concentrations at 4.0 hr 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 urea, induced a significant increase in serum LH 5 hr 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 LH within the limbic-preoptic area.