PLASMA-LEVELS OF LUTEINIZING-HORMONE DURING HYPERPROLACTINEMIA - RESPONSE TO CENTRAL ADMINISTRATION OF ANTAGONISTS OF CORTICOTROPIN-RELEASING FACTOR

Since high concentrations of prolactin (PRL) enhance the hypothalamic release of corticotropin-releasing factor (CRF), and CRF decreases the hypothalamic secretion of luteinizing hormone (LH)-releasing hormone (LHRH), it could be that CRF is involved in the suppressed secretion o f LH during hyperprolactinemia. The aim of this study was to explore t his possibility in hyperprolactinemic male rats. Hyperprolactinemia, i nduced by insertion of 3 pituitary glands under the kidney capsule, de creased plasma LH levels by 68% and caused a 2-fold increase in plasma corticosterone. Intracisternal administration of the CRF antagonist a lpha-helical CRF(9-41) induced both in pituitary-grafted rats and in n ormoprolactinemic controls a 2 to 3-fold increase of LH in the plasma sample taken 1 h after injection of alpha-helical CRF(9-41). Plasma le vels of LH in pituitary-grafted rats were 2-3 times higher during intr acerebroventricular infusion for 7 days with CRF antiserum than during saline infusion. Furthermore, after infusion of CRF antiserum for 7 d ays into the lateral brain ventricle plasma LH levels had increased by 270% in normoprolactinemic male rats. These results indicate that hyp othalamic CRF is involved in the control of LH release in male rats. T o further investigate whether CRF is involved in the effect of PRL on LH secretion, we infused PRL, alone or together with CRF antiserum, fo r 7 days into the lateral brain ventricle of normoprolactinemic male r ats. After 7 days of PRL infusion, LH levels had decreased by 45%, whe reas plasma corticosterone was 150% higher. This action of PRL on LH a nd corticosterone was prevented when besides PRL also CRF antiserum wa s infused. On the basis of these results it is suggested that the redu ced secretion of LH and the increased secretion of corticosterone duri ng hyperprolactinemia is at least partly due to a direct effect of PRL on the hypothalamus. Furthermore, hypothalamic CRF seems involved in the control of LH secretion, and hyperprolactinemia may enhance the hy pothalamic activity of CRF-producing neurons.