Subcutaneous implantation of a silastic tubing containing crystalline estradiol in castrated female rats results in a circadian rhythm of LH release. Under such conditions, blockade of serotonin (5-HT) biosynthesis by p-chlorophenylalanine (PCPA) completely inhibits the afternoon elevation of plasma LH. Gonadotropin peaks remain inhibited as long as the concentration of the transmitter is effectively depleted. Intraperitoneal administration or intraventricular infusion of minute doses of the immediate precursor of the amine, 5-hydroxytryptophan (5-HTP), results in the reappearance of the next afternoon rise of plasma gonadotropin, whenever hypothalamic levels of 5-hydroxyindole acetic acid (5-HIAA), the main metabolite of 5-HT, are significantly increased over their value in PGPA-treated animals. The administration of methiothepin, a 5-HT receptor blocker, 9 hours of more prior to the next expected LH rise, similarly inhibits the cycle, whereas a dopamine receptor inhibitor has no effect under the same time conditions. We have concluded that serotoninergic neuron systems can have a positive, permissive effect on the transfer of neural information resulting in phasic gonadotropin release; this action of the amine is different from, but not contradictory to, the known inhibitory effect of 5-HT on the release of LHRH from the median eminence.