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Submitted on December 2, 2004
Accepted on March 9, 2005
)-selective ligands induce galanin expression within gonadotropin hormone-releasing hormone-immunoreactive (GnRH-i) neurons in the female rat brain
Women's Health Research Institute, Wyeth Research, Collegeville, PA 19426, USA (IM and MVL) and Department of Anatomy & Neurobiology, University of Maryland, School of Medicine, Baltimore, BA 21201, USA (GEH)
* To whom correspondence should be addressed. E-mail: imerchem{at}epi.umaryland.edu.
Among the many factors that integrate the activity of the gonadotropin hormone-releasing hormone (GnRH) neuronal system, estrogens play the most important role. In females, estrogen, in addition to the negative feedback, also exhibits a positive feedback influence upon the activity and output of GnRH neurons to generate the preovulatory LH surge and ovulation. Until recently, the belief has been that the GnRH neurons do not contain estrogen receptors and that the action of estrogen upon GnRH neurons is indirect involving several, estrogen-sensitive neurotransmitter and neuromodulator systems that trans-synaptically regulate the activity of the GnRH neurons.
Based on our recent findings that GnRH neurons of the female rat co-express galanin, that galanin is a potent GnRH releasing peptide, and that estrogen receptor-
(ER) is present in GnRH neurons, we have evaluated the effect of 17-estradiol and two ER-selective agonists (WAY-070, WAY-818) on the expression of galanin within GnRH neurons. By combining immunocytochemistry for GnRH and in situ hybridization histochemistry for galanin, we demonstrate that 17-estradiol (20 µg/kg, sc) stimulates galanin expression within GnRH-i neurons in a time-dependent manner. A significant increase was observed two hours following its administration to ovariectomized rats. However, a more robust expression required 3 days treatment regimen. Treatment with the -selective ligands resulted similar observations, although no statistical analysis is available for the two hrs survival. These observations strongly suggest that estrogen and the ER-selective ligands stimulate galanin expression within GnRH neurons via ER, although an indirect mechanism via interneurons still cannot be ruled out.
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