Estrogen stimulates galanin expression within luteinizing hormone- releasing hormone-immunoreactive (LHRH-i) neurons via estrogen receptor-beta (ERbeta) in the female rat brain.
Among the many factors that integrate the activity of the luteinizing hormone-releasing hormone (LHRH) neuronal system, estrogens play the most important role. Until recently, the belief has been that the LHRH neurons do not contain estrogen receptors and that the action of estrogen upon LHRH neurons is indirect involving several, estrogen-sensitive neurotransmitter and neuromodulator systems that regulate the activity of the LHRH neurons. Based on our recent findings that LHRH neurons of the female rat co-express galanin, that galanin is a potent LHRH releasing peptide, and that estrogen receptor-beta (ERbeta) is present in LHRH neurons, we have evaluated the effect of 17beta-estradiol on the expression of galanin within LHRH neurons. By combining immunocytochemistry for LHRH and in situ hybridization histochemistry for galanin, we demonstrate that 17beta-estradiol stimulates galanin expression within 2h following their administration to ovariectomized rats. Maximal expression, however, required a longer treatment regimen (3 days). These observations strongly suggest that estrogens stimulate galanin expression within LHRH neurons directly, via ERbeta. Moreover, ERbeta may mediate, at least in part, the positive feedback effect of estrogens during the preovulatory LHRH and subsequent LH surges.[1]References
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