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

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Abstract
Injections of 2 mg of progesterone [P] into ovariectomized estrogen-primed rats significantly increased serum LH [lutropin] and FSH [follitropin] concentrations 3, 5 and 8 h later. Receptor blockers of noradrenaline (NA [norepinephrine]), dopamine (DA) or acetylcholine (ACH), phenoxybenzamine (20 mg/kg body wt), pimozide (1 mg/kg body wt), pimozide (1 mg/kg body wt) or atropine (700 mg/kg body wt), respectively, prevented the P-induced gonadotropin release. None of them blocked the gonadotropin release following unilateral electrochemical stimulation (100 .mu.A for 60 s) of the medial preoptic area which occurred 0.5 and 1.5 h later, although pimozide or atropine reduced serum LH concentrations at 4.0 h 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 LH 5 h 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 3 substances into the lateral septum induced LH release. All of NA, DA and ACH may play stimulaatory roles in the regulation of gonadotropin secretion and there are regional differences of their effectivenesses in releasing LH within the limbic-preoptic area.

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