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Submitted on November 19, 2002
Accepted on October 21, 2003
1 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston Texas USA
* To whom correspondence should be addressed.
Pituitary adenylate cyclase-activating polypepide (PACAP) regulates the secretion of GnRH (GnRH) into the hypothalamic hypophysial portal system and sensitizes the pituitary for release of hormones that trigger ovulation. Since reproductive behavior is synchronized with GnRH release, the present study was undertaken to determine whether PACAP in the VMN plays a role in receptivity. To this end, we used rat and mouse reproductive behavioral models to determine the biological relationship between PACAP and steroid receptor function in females. We provide evidence for the requirement of PACAP in the VMN for progesterone (P)-dependent sexual behavior in estrogen (E)-primed females. We clarify the biological and molecular mechanisms of PACAP activity by showing (1) that inhibition of endogenous PACAP suppresses P receptor (PR)-dependent sexual behavior facilitated by the steroid P or D1-like agonist SKF38393 and (2) that PR, steroid receptor coactivators (SRC-1 and SRC-2), and new protein synthesis are essential for ligand independent PACAP-facilitated behavior. These findings are consistent with convergence of PACAP-mediated cellular signals on PR for genomic activation and subsequent behavioral changes. Further, we show that steroids regulate both endogenous PACAP mRNA in the VMN and irPACAP in the medial basal hypothalamus (MBH) and cerebral spinal fluid (CSF) for ligand-dependent, steroid receptor-dependent receptivity. The present findings delineate a novel, steroid-dependent mechanism within the female hypothalamus by which the neuropeptide PACAP acts as a feed-forward, paracrine and/or autocrine factor for synchronization of behavior coordinate with hypothalamic control of ovulation.
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