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Central and Peripheral Effects of RFamide-Related Peptide-3 on Luteinizing Hormone and Prolactin Secretion in Rats

Centre for Neuroendocrinology and Departments of Anatomy and Structural Biology (G.M.A., H.-L.R., M.Z.R.) and Obstetrics and Gynaecology (J.J.E.), University of Otago, Dunedin 9054, New Zealand

Address all correspondence and requests for reprints to: Dr. Greg Anderson, Centre for Neuroendocrinology and Department of Anatomy and Structural Biology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin 9054, New Zealand. E-mail: greg.anderson{at}anatomy.otago.ac.nz.

Hypothalamic RFamide-related peptide-3 (RFRP-3) neurons inhibit LH secretion via a central action. A direct hypophysiotropic action on the gonadotropes has also been suggested. To assess central RFRP-3 effects on the GnRH/LH surge that induces ovulation, ovariectomized rats were subjected to an estradiol plus progesterone surge-induction protocol. Chronic infusion of RFRP-3 (2.5 or 25 ng/h, intracerebroventricularly) caused a dose-dependent 50–60% inhibition of GnRH neuronal activation (assessed by colocalization with the immediate early gene c-Fos) at the surge peak compared with vehicle-treated controls. RFRP-3 also suppressed neuronal activation in the anteroventral periventricular region, which provides stimulatory input to GnRH neurons, by 50–80% compared with control values. To test whether centrally administered RFRP-3 inhibits pulsatile GnRH/LH secretion, chronically ovariectomized, low-level estradiol-treated rats without surge induction were blood sampled every 10 min for 4 h. Bolus injection of RFRP-3 (0, 2.5, or 25 µg, intracerebroventricularly) after 1.5 h did not affect subsequent LH pulse frequency, pulse amplitude, or the mean concentrations of LH or prolactin. RFRP-3 treatment of isolated anterior pituitary cells at moderate doses of up to 10^–7 M did not significantly inhibit LH release, either with or without GnRH cotreatment. These data reveal a central inhibitory effect of RFRP-3 on the hypothalamo-pituitary gonadal axis specifically during the estradiol-induced GnRH/LH surge. This effect may include actions of RFRP-3 on GnRH neurons and/or their anteroventral periventricular afferent inputs but is unlikely to involve direct inhibition of LH secretion at the level of the gonadotrope.

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