Evidence for an Inhibitory Dopaminergic and Stimulatory Noradrenergic Hypothalamic Influence on PMS-Induced Ovulation in the Immature Rat. II. A Pharmacological Analysis

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Abstract
Pregnant mare''s serum gonadotropin (PMS; 10 IU day 30)-induced ovulation was used as a model to study the effect of drugs interfering with monoamine neurotransmission on CNS processes controlling ovulation. Drugs were administered during the critical period on day 32, and tubal eggs were counted in the morning of day 33. When injected during the critical period, dopamine (DA) receptor agonists such as apomorphine, ET 495 [pyrimidylpiperonyl piperazine] ergotamine, 2-bromo-.alpha.-ergocryptine, lergotrile and ergocornine inhibited ovulation, an effect which was counteracted by the DA receptor blocking agent, pimozide. By itself, pimozide had no significant effect, whereas combined noradrenaline (norepinephrine, NA) and DA receptor blocking agents such as chlorpromazine and clozapine inhibited ovulation. .alpha.- and .beta.-adrenergic blocking agents and drugs influencing 5-hydroxytryptamine (5-HT) neurotransmission did not affect ovulation. LH-RH [luteinizing hormone-releasing hormone] removed the ovulatory blockade induced by ET 495 in the same dose-range as it removed pentobarbital-induced blockade of ovulation. Ergocornine did not block ovulation after the critical period and was less effective when given prior to the critical period. The DA receptor agonists may act via a central action. There may be a central inhibitory DA and facilitory NA mechanism in the control of PMS-induced ovulation in the immature female rat.