Suppression of Prolactin Secretion by Benzodiazepines in vivo

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Abstract
Administration of benzodiazepines to male or female rats was observed to inhibit prolactin release. Basal secretion of prolactin was only slightly suppressed with the highest dose of benzodiazepines; however, the rise in prolactin release following a stimulus was prevented even at low doses (0.1–1 mg/kg). The benzodiazepine diazepam blocked stress-induced prolactin release and, when given during the critical period of proestrus, the proestrus surge of prolactin. Diazepam administration also blunted the release of prolactin induced by dopaminergic receptor blockade following haloperidol, or by serotonergic receptor activation produced by fluoxetine, a serotonergic reuptake inhibitor plus 5-hydroxytryptophan, a serotonin precursor. Inhibition of prolactin release by benzodiazepine was dose related, and inhibition was still evident after repeated diazepam injection. The potency of three benzodiazepine analogues to inhibit prolactin release correlated with their potency to displace radiolabeled diazepam binding from brain membrane fractions or to induce other biological responses (clonazepam > diazepam > chlordiazepoxide). These actions of benzodiazepines on prolactin release are similar to those reported for γ-aminobutyric acid (GABA). The hypothesis of a benzodiazepine GABA receptor complex suggests that GABA may be involved in these in vivo actions of diazepam.