Endogenous opioid peptides participate in the modulation of prolactin release in response to cervicovaginal stimulation in the female rat.

Naloxone, a specific opiate receptor antagonist, was used to evaluate the influence of endogenous opiate peptides on PRL secretion during various stages of the estrous cycle and after cervicovaginal stimulation. Naloxone (0.2 mg/kg, iv) administered at 0930 h suppressed basal 1000 h PRL levels on each day of the estrous cycle, but had no effect on the PRL surges occurring on the afternoon of proestrus and estrus. These afternoon surges could only be suppressed when naloxone was given immediately before the onset of the surge at 1330 h, suggesting a critical period for naloxone action. Later injections (at 1530 and 1730 h) had no further suppressive effects, although these injections suppressed the basal PRL secretion occurring during diestrous days I and II to near undetectable levels. In contrast, the immediate (1000 h) and afternoon PRL discharges triggered by cervicovaginal stimulation at 0930 h on proestrus, estrus, and diestrous day I were significantly suppressed by a single injection of naloxone, but only when it was administered before application of the stimulus. Moreover, this single naloxone injection significantly inhibited the long term PRL surges occurring during days 2 and 4 of pseudopregnancy in animals stimulated on estrus and diestrous day I. Naloxone treatment significantly shortened the duration of pseudopregnancy but did not prevent it, indicating that only minimal levels of PRL may be necessary to initiate and maintain pseudopregnancy. This striking difference in the time at which naloxone suppressed the stimulus-induced PRL discharges (compared to the spontaneous surges) suggests that endogenous opiate peptides also process the sensory information necessary for establishment of PRL surges during pseudopregnancy. The marked dependence of the spontaneous as well as the stimulus-induced PRL discharges on the stage of the estrous cycle support established evidence that ovarian steroids enhance endogenous opiate activity or facilitate the transfer of information along opiatergic pathways for the generation of PRL surges.