Neuroscience 2001 Abstract
| Presentation Number: | 628.5 |
|---|---|
| Abstract Title: | Role of estrogen receptor-β (ER-β) in regulating neurohypophyseal hormone release in vitro. |
| Authors: |
Somponpun, S. J.*1
; Sladek, C. D.1
1Dept Physiol & Biophysics, FUHS/Chicago Med Sch, Chicago, IL |
| Primary Theme and Topics |
Autonomic, Limbic and Other Systems - Neuroendocrine -- Steroid/brain interactions |
| Secondary Theme and Topics | Autonomic, Limbic and Other Systems<br />- Neuroendocrine<br />-- Other |
| Session: |
628. Neuroendocrine: steroid/brain interactions VI Poster |
| Presentation Time: | Tuesday, November 13, 2001 1:00 PM-2:00 PM |
| Location: | Exhibit Hall KK-2 |
| Keywords: | vasopressin, oxytocin, supraoptic, NMDA |
Supraoptic neurones are regulated by estrogen (E2) and express ER-β. Physiological concentrations of E2 inhibit NMDA-stimulated vasopressin (VP) release from explants of the hypothalamo-neurohypophyseal systems. To test the hypothesis that this effect of E2 is mediated by ER-β, tetrahydrochrysene, R,R-enantiomer (R,R-THC), a compound which is an ER-β antagonist and an ER-α agonist was used (1). Explants from male Sprague-Dawley rats (129-150g, n=5-7/group) were perifused and hormone release was measured in timed fractions by radioimmunoassay. Following a 4hr equilibration period, explants were either exposed to 50μM NMDA for 3hrs. or maintained in basal medium. E2 (50pg/ml) and/or R,R-THC (55.2nM, a 300fold excess relative to E2) were present in the medium of some explants throughout the entire perifusion. At this concentration, R,R-THC did not alter basal VP release. In basal medium, NMDA caused an increase in VP release that was significantly elevated compared to control explants for approximately 1hr (p<0.05). This effect was blocked by E2 (p<0.05), but not by R,R-THC alone. Thus, R,R-THC did not interfere with the VP response to NMDA. Since R,R-THC has an ER-α agonist activity this suggests that the inhibitory effect of E2 on NMDA-induced VP release is not mediated by ER-α. The inhibitory effect of E2 was reversed in the presence of R,R-THC (p<0.05). Since R,R-THC is an ER-β antagonist its ability to restore the response to NMDA is consistent with the inhibitory effect of E2 being mediated by ER-β. (1) Sun et al. Endocrinology 140, 800-804,1999. R,R-THC provided by J A Katzenellenbogen.
Supported by NIH RO1NS27975
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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