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  • Title: Plasma levels of luteinizing hormone during hyperprolactinemia: response to central administration of antagonists of corticotropin-releasing factor.
    Author: de Greef WJ, Ooms MP, Vreeburg JT, Weber RF.
    Journal: Neuroendocrinology; 1995 Jan; 61(1):19-26. PubMed ID: 7731494.
    Abstract:
    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 of LH during hyperprolactinemia. The aim of this study was to explore this possibility in hyperprolactinemic male rats. Hyperprolactinemia, induced by insertion of 3 pituitary glands under the kidney capsule, decreased plasma LH levels by 68% and caused a 2-fold increase in plasma corticosterone. Intracisternal administration of the CRF antagonist alpha-helical CRF(9-41) induced both in pituitary-grafted rats and in normoprolactinemic 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 levels of LH in pituitary-grafted rats were 2-3 times higher during intracerebroventricular infusion for 7 days with CRF antiserum than during saline infusion. Furthermore, after infusion of CRF antiserum for 7 days into the lateral brain ventricle plasma LH levels had increased by 270% in normoprolactinemic male rats. These results indicate that hypothalamic CRF is involved in the control of LH release in male rats. To further investigate whether CRF is involved in the effect of PRL on LH secretion, we infused PRL, alone or together with CRF antiserum, for 7 days into the lateral brain ventricle of normoprolactinemic male rats. After 7 days of PRL infusion, LH levels had decreased by 45%, whereas plasma corticosterone was 150% higher. This action of PRL on LH and corticosterone was prevented when besides PRL also CRF antiserum was infused.(ABSTRACT TRUNCATED AT 250 WORDS)
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