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LA Bero and CM Kuhn
The goal of this study was to determine if the opioid system which is stimulatory to prolactin (PRL) secretion develops before the serotonergic system which regulates PRL release. The opioid and serotonergic systems were chosen for comparison because evidence exists that functional serotonergic neurons are necessary for opiate-induced PRL secretion in adult rats. Haloperidol and morphine produced a dose- related stimulation of PRL release in animals of all ages. In contrast, the serotonin agonists, quipazine and m-chlorophenylpiperazine, and the serotonin-releasing drug p-chloroamphetamine produced dose-related increases in PRL release in adult rats, but not in neonatal rats. The PRL response to the serotonin precursor 5-hydroxytryptophan was potentiated by fluoxetine only in animals 15 days of age or older. PRL secretion induced by these serotonergic agents was blocked by cyproheptadine, a serotonin receptor antagonist. Unlike PRL, corticosterone and growth hormone secretion were stimulated by quipazine and 5-hydroxytryptophan plus fluoxetine in both adult and neonatal rats. These findings suggest that stimulatory opioid control of PRL secretion and the dopaminergic mechanism which tonically inhibits PRL release are intact in the neonatal rat. In contrast, the stimulatory serotonergic mechanism is not functional until between 10 to 15 days of age. This late maturation appears to be specific to the serotonergic neurons regulating PRL release because the corticosterone and growth hormone responses to serotonergic stimulation develop early in ontogeny.
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