INVOLVEMENT OF NEURONES CONTAINING 5-HYDROXYTRYPTAMINE IN THE MECHANISM OF PROLACTIN RELEASE INDUCED BY OESTROGEN

Abstract

SUMMARY Oestradiol benzoate (OB) injected into spayed rats induced high levels of serum prolactin (measured by radioimmunoassay) in the afternoon of the third day after the injection. When progesterone was injected into spayed rats primed 3 days before with OB, a release of prolactin was observed in the morning. These rises in serum prolactin were prevented either by treatment with p-chlorophenylalanine (PCPA), a compound which depletes 5-hydroxytryptamine (5-HT) from the brain or by injecting the 5-HT antagonist methysergide, into the third ventricle. The blockade of prolactin release by PCPA treatment of OB-injected rats was partially reversed by the administration of 5-hydroxytryptophan. These results indicate that 5-HT containing neurones mediate the effect of ovarian steroids on prolactin release. Further support of this view was provided by experiments showing that the injection of 5-HT into the third ventricle raised serum prolactin levels. The rise in serum prolactin observed after the ovarian steroid treatment was blocked to a great extent by the injection of picrotoxin or strychnine. Picrotoxin also blocked the rise in serum prolactin induced by the injection of 5-HT into the third ventricle but failed to affect the rise in serum prolactin after i.v. injection of thyrotrophin-releasing hormone or α-methyl-p-tyrosine treatment. The results suggest that an inhibitory neuronal mechanism mediated by 5-HT neurones is involved in the release of prolactin induced by ovarian steroids.