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Stress-Induced Suppression of the Gonadotropin-Releasing Hormone Pulse Generator in the Female Rat: A Novel Neural Action for Calcitonin Gene-Related Peptide

Centre for Reproduction, Endocrinology and Diabetes (J.E.B., J.C.M., K.T.O., X.F.L.) and Centre for Cardiovascular Biology & Medicine (S.D.B.), New Hunt’s House King’s College London, Guy’s Campus, London SE1 1UL, United Kingdom; and Henry Wellcome Laboratory for Integrative Neuroscience & Endocrinology (S.L.L.), Dorothy Hodgkin Building, University of Bristol, Bristol BS1 3NY, United Kingdom

Address all correspondence and requests for reprints to: Dr. X. F. Li, Centre for Reproduction, Endocrinology and Diabetes, 2.36 New Hunt’s House, King’s College London, Guy’s Campus, London SE1 1UL, United Kingdom. E-mail: xiao_feng.li{at}kcl.ac.uk.

In addition to its role as a potent vasodilator, calcitonin gene-related peptide (CGRP) is centrally involved in a variety of stress responses, including activation of the hypothalamo-pituitary-adrenocortical axis. It is well known that stress suppresses the activity of the hypothalamic GnRH pulse generator, the central regulator of LH and FSH pulses, resulting in reproductive dysfunction. The aim of this study was to test the hypothesis that CGRP has a critical role in mediating stress-induced suppression of pulsatile LH secretion in the rat. Ovariectomized rats were implanted with intracerebroventricular and iv cannulae. Central administration of CGRP (75 pmol–1.2 nmol) into the lateral cerebral ventricle resulted in a profound, dose-dependent suppression of LH pulses, which was reversed by a CGRP receptor antagonist (CGRP_8–37,1 nmol). Although the site of action of CGRP remains to be established, the induction of c-Fos expression in the preoptic area and hypothalamic paraventricular nucleus might suggest an involvement of these brain regions. Intravenous administration of CGRP did not affect LH pulses. Coadministration (intracerebroventricular) of CGRP (400 pmol) with a CRH antagonist (-helical CRF_9–41, 26 nmol) partly blocked the CGRP-induced suppression of LH pulses. Furthermore, CGRP_8–37 (1 nmol) completely blocked hypoglycemic stress-induced suppression of LH pulses. These results suggest that the suppression of pulsatile LH secretion by central administration of CGRP may be mediated in part by CRH, and that CGRP may play a pivotal role in the normal physiological response of stress-induced suppression of the hypothalamic GnRH pulse generator, and hence the reproductive system.

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