Endocrinology, Vol 121, 127-132, Copyright © 1987 by Endocrine Society

ARTICLES

Intracerebroventricular injection of cholecystokinin octapeptide elevates plasma prolactin levels through stimulation of vasoactive intestinal polypeptide

K Tanimoto, CA Tamminga, TN Chase and G Nilaver

We investigated the effect of cholecystokinin octapeptide (CCK-8) on plasma PRL levels in freely moving male rats. Intravenous injection of CCK-8 did not affect basal plasma PRL levels in doses up to 5000 ng/rat; however, plasma PRL increased significantly after intracerebroventricular (icv) injection of the peptide at a dose of 40 ng/rat. Proglumide (0.2 mg/kg, iv) and benzotript (0.2 mg/kg, iv), specific CCK receptor antagonists, blocked the icv CCK-8-induced increase in plasma PRL levels. There was no apparent effect of icv CCK- 8 on the enhancement of PRL release by haloperidol (0.2 mg/kg, iv), sulpiride (0.1 mg/kg, iv), domperidone (0.1 mg/kg, iv), or RO22-1319 (0.1 mg/kg, iv). However, the apomorphine-induced inhibition of PRL secretion was significantly antagonized by icv CCK-8. Furthermore, icv CCK-8 increased plasma PRL levels in rats depleted of dopamine by pretreatment with reserpine and alpha-methyl-p-tyrosine. Finally, the elevation in plasma PRL levels produced by icv CCK-8 was substantially antagonized by vasoactive intestinal polypeptide antiserum (1:3; 10 microliter/rat, icv). These results suggest that CCK-8 increases plasma PRL through an interaction with a central CCK receptor, which stimulates the activity of vasoactive intestinal polypeptide, a putative PRL-releasing factor.

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