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Role of Estrogen Receptor-ß in Regulation of Vasopressin and Oxytocin Release in Vitro

Department of Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, Colorado 80262

Address all correspondence and requests for reprints to: Celia D. Sladek, Ph.D., Department of Physiology and Biophysics, University of Colorado Health Science Center, 4200 East Ninth Avenue, Denver, Colorado 80262. E-mail: . celia.sladek{at}uchsc.edu

In rats, the magnocellular neurons that produce vasopressin (VP) and oxytocin (OT) express estrogen receptor-ß (ER-ß). Physiological concentrations of estrogen (E2) inhibit N-methyl-D-aspartate (NMDA)-stimulated VP and OT release from explants of the hypothalamo-neurohypophyseal system (HNS). To determine whether ER-ß mediates inhibition by E2, HNS explants were perifused with and without NMDA (50 µM) in the presence of E2 (50 pg/ml), E2 coupled to BSA (E2:BSA), genistein (100 nM, a phytoestrogen with affinity for ER-ß), or tetrahydrochrysene-R,R,-enantiomer (R,R-THC, a ligand that acts as an agonist on ER- but an antagonist on ER-ß). VP and OT released into the perifusate were measured by RIA. E2 and genistein inhibited NMDA-stimulated VP release, but E2:BSA and R,R,THC were not effective inhibitors. However, R,R,THC blocked E2 inhibition of NMDA-stimulated VP release. The inability of E2:BSA to mimic the effect of E2 indicates that E2 inhibition is not mediated by membrane receptors. The ability of genistein to mimic the effect of E2 suggests that the effect is mediated by ERß. This interpretation is supported by the ability of R,R,THC to block but not to mimic the effect of E2. Thus, E2 inhibition of NMDA-stimulated VP and OT release may be mediated by ER-ß.

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