This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parent, A.-S. Articles by Bourguignon, J.-P. Search for Related Content PubMed PubMed Citation Articles by Parent, A.-S. Articles by Bourguignon, J.-P. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH Hazardous Substances DB OXYTOCIN

Oxytocin Facilitates Female Sexual Maturation through a Glia-to-Neuron Signaling Pathway

Developmental Neuroendocrinology Unit (A.-S.P., G.R., M.-C.L., A.G., J.-P.B.), University of Liège, 4000 Liège, Belgium; and Division of Neuroscience (V.M., A.L., S.R.O.), Oregon National Primate Research Center, Beaverton, Oregon 97006

Address all correspondence and requests for reprints to: Jean-Pierre Bourguignon, Developmental Neuroendocrinology Unit, CHU Sart Tilman, 4000 Liège, Belgium. E-mail: jpbourguignon{at}ulg.ac.be.

It has been earlier proposed that oxytocin could play a facilitatory role in the preovulatory LH surge in both rats and humans. We here provide evidence that oxytocin also facilitates sexual maturation in female rats. The administration of an oxytocin antagonist for 6 d to immature female rats decreased GnRH pulse frequency ex vivo and delayed the age at vaginal opening and first estrus. The in vitro reduction in GnRH pulse frequency required chronic blockade of oxytocin receptors, because it was not acutely observed after a single injection of the antagonist. Hypothalamic explants exposed to the antagonist in vitro showed a reduced GnRH pulse frequency and failed to respond to oxytocin with GnRH release. Prostaglandin E₂ (PGE₂) mimicked the stimulatory effect of oxytocin on GnRH pulse frequency, and inhibition of PG synthesis blocked the effect of oxytocin, suggesting that oxytocin accelerates pulsatile GnRH release via PGE₂. The source of PGE₂ appears to be astrocytes, because oxytocin stimulates PGE₂ release from cultured hypothalamic astrocytes. Moreover, astrocytes express oxytocin receptors, whereas GnRH neurons do not. These results suggest that oxytocin facilitates female sexual development and that this effect is mediated by a mechanism involving glial production of PGE₂.

This article has been cited by other articles:

				J. A. Mennigen, C. J. Martyniuk, K. Crump, H. Xiong, E. Zhao, J. Popesku, H. Anisman, A. R. Cossins, X. Xia, and V. L. Trudeau Effects of fluoxetine on the reproductive axis of female goldfish (Carassius auratus) Physiol Genomics, November 12, 2008; 35(3): 273 - 282. [Abstract] [Full Text] [PDF]