OPIOID REGULATION OF PROLACTIN SECRETION: EVIDENCE FOR A SPECIFIC ROLE OF β-ENDORPHIN

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Abstract
Previous studies have shown that exogenously administered opioids, including β-endorphin, stimulate prolactin release. The fact that naloxone has been shown to lower baseline and stress-induced serum prolactin in rats suggests that endogenous opioids may participate in prolactin regulation, but does not specify which opioid is involved. In a previous study we showed that intravenously administered anti-β-endorphin antiserum had no effect on either baseline or stress-induced prolactin release in rats. In the present study we have repeated our earlier experiments, but have given the antiserum into the cerebral ventricles rather than intravenously. Significant lowering of baseline serum prolactin, to 56.6% ± 10.6% (SEM) that of controls (p<0.005), was noted. Also noted was blunting of the stress-induced prolactin rise, to 69.2% ± 6.7% that of controls (p<0.002). These results indicate that β-endorphin is specifically involved in both the tonic and stress-mediated release of prolactin. Because the magnitude of prolactin lowering with antiserum was at least as great as what we had earlier observed with naloxone, they suggest that g-endorphin is the major and possibly the sole opioid involved in prolactin regulation. They also indicate that the previous lack of effect of anti-β-endorphin antiserum on serum prolactin was due to its failure, after intravenous administration, to achieve effective concentrations at critical controlling sites within the brain.