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Am J Physiol Regul Integr Comp Physiol 291: R53-R58, 2006; doi:10.1152/ajpregu.00766.2005
0363-6119/06 $8.00
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Neurohypophyseal Hormones:From Genomics and Physiology to Disease

Oxytocin receptor binding in the hypothalamus during gestation in rats

Steven L. Bealer, David L. Lipschitz, Gina Ramoz, and William R. Crowley

Department of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, Utah

Submitted 31 October 2005 ; accepted in final form 1 February 2006

Central oxytocin receptors (OTR) may be involved in adaptations of the brain oxytocin (OT) system during gestation, which are critical for systemic release of OT during parturition and lactation. We used quantitative autoradiography to determine changes in OTR binding in numerous brain sites during the course of gestation in the rat. Furthermore, to evaluate the importance of ovarian steroids in mediating pregnancy-related changes in OTR binding, we measured binding in ovariectomized animals treated with progesterone and/or estrogen, and in pregnant animals treated with exogenous progesterone during late gestation. We found that OTR binding was significantly increased in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) by midgestation (day 15) compared with control. In addition, there was a further significant increase in OTR binding in these nuclei by late gestation (day 20). The bed nucleus of the stria terminalis (BNST) and the medial preoptic area (MPOA) also showed significant gestation-associated increases in OTR binding, which were similar during mid- and late pregnancy. Treatment with exogenous progesterone throughout pregnancy did not alter the increase in OTR binding characteristic of late gestation in any of these brain sites. Finally, estrogen treatment in ovariectomized animals resulted in increased OTR binding in the SON, BNST, and MPOA, but not the PVN. These data demonstrate that OTR binding in the hypothalamus is increased during mid- and late-gestation, compared with ovariectomized control animals, which may be mediated by increased estradiol.

estrogen; progesterone; steroids; ovariectomy



Address for reprint requests and other correspondence: S. L. Bealer, Dept. of Pharmacology and Toxicology, Univ. of Utah, 30 South 2000 East Rm. 201, Salt Lake City, UT 84121 (E-mail: steve.bealer{at}deans.pharm.utah.edu)




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