Monoamines and Ovulation in the Rat

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Abstract
A study was made of the possible involvement of monoamine''rgic pathways in the neural mechanisms which activate the adenohypophysis to release ovulating hormone. Practically no animals ovulated after treatment with re-serpine (5 mg/kg subcut), and a 1 mgAg dose inhibited ovulation in 50%. In agreement with earlier data, blockade of ovulation occurred only when reserpine was administered prior to the assumed critical period of LH [luteinizing hormone] release and not if the injection was given immediately afterward. The inhibitory effect to reserpine on ovulation was prevented by treatment with either of the monoamin''e oxidase inhibitors, pargyline (25 mgAg subcut) or nialamide (200 mgAg subcut). Experiments involving treatment with nialamide or nialamide-DOPA on the morning of proestrus, combined with hypophysectomy at different times during the critical period for LH discharge, revealed that increased monoamine levels did not advance the time of LH release. Pargyline itself, at a dosage of 50 mgAg sc, blocked ovulation, and on the day following treatment uterine weights were increased over controls. Both effects were obtained only if the compound was given before the critical period and not when administered immediately afterward. Blocking dosages of reserpine, however, did not effect increases in uterine weight. Experiments with pargyline in combination with the monoamine precursors DOPA and 5-HTP [5 hydroxytrypt-amine] indicate that the effects of pargyline on ovulation and uterine weight are not brought about by increased monoamine levels even though intact monoaminergic pathways appear to be necessary for triggering the ovulatory discharge of LH.