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Endocrinology Vol. 146, No. 7 2976-2984
Copyright © 2005 by The Endocrine Society

Differential Regulation of KiSS-1 mRNA Expression by Sex Steroids in the Brain of the Male Mouse

Jeremy T. Smith, Heather M. Dungan, Elizabeth A. Stoll, Michelle L. Gottsch, Robert E. Braun, Stephen M. Eacker, Donald K Clifton and Robert A. Steiner

Departments of Physiology and Biophysics (J.T.S., H.M.D., M.L.G., R.A.S.), Genome Sciences (R.E.B., S.M.E.), and Obstetrics and Gynecology (D.KC., R.A.S.), and the Graduate Program in Neurobiology and Behavior (E.A.S.), University of Washington, Seattle, Washington 98195-7290

Address all correspondence and requests for reprints to: Robert A. Steiner, Department of Physiology and Biophysics, Health Sciences Building, G-424, School of Medicine, University of Washington, Box 357290, Seattle, Washington 98195-7290. E-mail: steiner{at}u.washington.edu.

Kisspeptins are products of the Kiss1 gene, which bind to GPR54, a G protein-coupled receptor. Kisspeptins and GPR54 have been implicated in the neuroendocrine regulation of GnRH secretion. To test the hypothesis that testosterone regulates Kiss1 gene expression, we compared the expression of KiSS-1 mRNA among groups of intact, castrated, and castrated/testosterone (T)-treated male mice. In the arcuate nucleus (Arc), castration resulted in a significant increase in KiSS-1 mRNA, which was completely reversed with T replacement, whereas in the anteroventral periventricular nucleus, the results were the opposite, i.e. castration decreased and T increased KiSS-1 mRNA expression. In the Arc, the effects of T on KiSS-1 mRNA were completely mimicked by estrogen but only partially mimicked by dihydrotestosterone, a nonaromatizable androgen, suggesting that both estrogen receptor (ER) and androgen receptor (AR) play a role in T-mediated regulation of KiSS-1. Studies of the effects of T on KiSS-1 expression in mice with either a deletion of the ER{alpha} or a hypomorphic allele to the AR revealed that the effects of T are mediated by both ER{alpha} and AR pathways, which was confirmed by the presence of either ER{alpha} or AR coexpression in most KiSS-1 neurons in the Arc. These observations suggest that KiSS-1 neurons in the Arc, whose transcriptional activity is inhibited by T, are targets for the negative feedback regulation of GnRH secretion, whereas KiSS-1 neurons in the anteroventral periventricular nucleus, whose activity is stimulated by T, may mediate other T-dependent processes.




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