Gonadotropin-Releasing Hormone Surge: Possible Modulation through Postsynaptic α-Adrenoreceptors and Two Pharmacologically Distinct Dopamine Receptors*

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Abstract
We have studied modulation of the release of gonadotropin-releasing hormone (GnRH) by central monoaminergic neurons. The test system was the GnRH surge that occurs at 1700 h on day 32 in female rats injected on day 30 with PMS gonadotropin (PMSG). The release of GnRH, measured by RIA of pituitary stalk blood, was correlated with the release of LH, measured by RIA of external jugular venous blood. All blood samples were collected under Althesin (alphaxalone plus alphadolone acetate) anesthesia. The heights of the PMSG-induced surges of GnRH and LH were reduced in animals which had been injected with either αmethyl-p-tyrosine (an inhibitor of tyrosine hydroxylase), or diethyldithiocarbamate or fusaric acid (inhibitors of dopamine-β-hydroxylase). The action of all three inhibitors was reversed by administering dihydroxyphenylserine, and the inhibitory action of diethyldithiocarbamate was potentiated by L-dopa, The height of the PMSG-induced LH surge was reduced by phenoxybenzamine, but was not affected by phentolamine, yohimbine, D,L- or D-propranolol, or clonidine. Phenoxybenzarriine also reduced significantly the height of the PMSG-induced GnRH surge. The heights of the GnRH and LH surges were increased by pimozide and domperidone and reduced by haloperidol. The action of all three of these dopamine receptor blockers could be reversed by apomorphine. Domperidone administered before the critical period on the afternoon of proestrus in adult rats also increased significantly the height of the spontaneous LH surge. These results show that the GnRH surge depends upon the functional integrity of central noradrenergic neurons which facilitate GnRH release, possibly through a-adrenoreceptors. The GnRH surge can be inhibited by dopamine acting on receptors that are blocked by pimozide and domperidone and facilitated by dopamine acting on receptors that are blocked by haloperidol. (Endocrinology108: 862, 1981)

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