Suckling-induced prolactin release is suppressed by naloxone and simulated by beta-endorphin.

The role that opiate peptides play in suckling-induced prolactin (PRL) release was examined in 10-day postpartum lactating rats. The opiate receptor antagonist naloxone (NAL) suppressed suckling-induced PRL release in a dose-dependent manner and a large dose abolished the response. These results suggest either that opiate neurons are situated in the neuronal pathway mediating this neuroendocrine response, or alternatively, that opiate neurons are situated such that they can modulate neuronal transmission in this pathway. It is suggested that NAL blocks a tonic, inhibitory beta-endorphinergic input to the tuberoinfundibular dopaminergic (TIDA) neurons, hence, NAL administration in effect stimulates the TIDA neurons and in this way overrides the suckling response. Intravenous, bolus administration of beta-endorphin (beta-END) produced a PRL response that was similar to the suckling response in terms of latency of onset and duration while the magnitude of the beta-END-induced response was 2-fold greater than that produced by the suckling stimulus. NAL abolished beta-END-induced PRL release at a much lower dose than that required to inhibit suckling-induced PRL release. This suggests that the neural mediation of the suckling response involves a mechanism in addition to the one inhibited by opiate receptor blockade.