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Submitted on July 23, 2004
Accepted on September 15, 2004
Division of Reproductive Health, Endocrinology and Development, New Hunt's House, King's College London, Guy's Campus, SE1 1UL, UK. Henry Wellcome Laboratory for Integrative Neuroscience & Endocrinology, Dorothy Hodgkin Building, University of Bristol, BS13NY, UK
* To whom correspondence should be addressed. E-mail: kevin.o'byrne{at}kcl.ac.uk.
CRF has been implicated as an important mediator of stress-induced inhibition of reproduction. The role of specific CRF receptor subtypes in this effect is unknown and in the current study we have investigated the role of the CRF-R2 receptor in stress-mediated suppression of pulsatile LH section. Ovariectomized rats with subcutaneous 17
-estradiol capsules were implanted with intracerebroventricular (icv) and intravenous cannulae. Blood samples (25 µl) were collected every 5 min for 5 h for LH measurement. Central administration of urocortin II (0.24, 2.4, 24 or 240 nmol, icv), which selectively binds to CRF-R2, resulted in a dose-dependent suppression of LH pulses. Restraint stress (1 h) induced a profound suppression of pulsatile LH secretion and astressin2-B, a selective CRF-R2 antagonist (28 nmol icv, 10-min pre-restraint), was effective in blocking this inhibitory response. These findings suggest that CRF-R2 mediates, at least in part, restraint stress-induced inhibition of LH pulses and 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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