PMID- 12764114 OWN - NLM STAT- MEDLINE DCOM- 20030625 LR - 20231013 IS - 1529-2401 (Electronic) IS - 0270-6474 (Print) IS - 0270-6474 (Linking) VI - 23 IP - 10 DP - 2003 May 15 TI - Osmotic regulation of estrogen receptor-beta in rat vasopressin and oxytocin neurons. PG - 4261-9 AB - The vasopressin (VP) magnocellular neurosecretory cells (MNCs) in the supraoptic and paraventricular (PVN) nuclei are regulated by estrogen and exhibit robust expression of estrogen receptor (ER)-beta. In contrast, only approximately 7.5% of oxytocin (OT) MNCs express ER-beta. We examined the osmotic regulation of ER-beta mRNA expression in MNCs using quantitative in situ hybridization histochemistry. Hyper-osmolality induced via 2% hypertonic saline ingestion significantly decreased, whereas sustained hypo-osmolality induced via d-d-arginine VP and liquid diet increased ER-beta mRNA expression in MNCs (p < 0.05). Thus, the expression of ER-beta mRNA correlated inversely with changes in plasma osmolality. Because hyper-osmolality is a potent stimulus for VP and OT release, this suggests an inhibitory role for ER-beta in MNCs. Immunocytochemistry demonstrated that the decrease in ER-beta mRNA was translated into depletion of receptor protein content in hyper-osmotic animals. Numerous MNCs were positive for ER-beta in control animals, but they were virtually devoid of ER-beta-immunoreactivity (IR) in hyper-osmotic animals. The osmotically induced decrease in ER-beta expression was selective for MNCs because ER-beta-IR remained unaltered in PVN parvocellular neurons. Plasma estradiol and testosterone were not correlated with ER-beta mRNA expression after osmotic manipulation, suggesting that ER-beta expression was not driven by ligand availability. Expression of FOS-IR in MNCs with attenuated ER-beta-IR, and the absence of FOS-IR in parvocellular neurons that retain ER-beta-IR suggest a role for neuronal activation in the regulation of ER-beta expression in MNCs. Thus, osmotic modulation of ER-beta expression in MNCs may augment or attenuate an inhibitory effect of gonadal steroids on VP release. FAU - Somponpun, Suwit J AU - Somponpun SJ AD - Department of Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. FAU - Sladek, Celia D AU - Sladek CD LA - eng GR - R01 NS027975/NS/NINDS NIH HHS/United States GR - NS27975/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Estrogen Receptor beta) RN - 0 (Hormones) RN - 0 (Receptors, Estrogen) RN - 11000-17-2 (Vasopressins) RN - 451W47IQ8X (Sodium Chloride) RN - 50-56-6 (Oxytocin) SB - IM MH - Animals MH - Blood Volume/physiology MH - Body Weight/physiology MH - Estrogen Receptor beta MH - Hematocrit MH - Hormones/blood/physiology MH - Hypernatremia/physiopathology MH - Hyponatremia/physiopathology MH - Male MH - Neurons/cytology/*metabolism MH - Osmolar Concentration MH - *Osmotic Pressure MH - Oxytocin/blood/*metabolism MH - Paraventricular Hypothalamic Nucleus/cytology/metabolism/physiology MH - Rats MH - Rats, Sprague-Dawley MH - Receptors, Estrogen/biosynthesis/genetics/*metabolism MH - Sodium Chloride/metabolism MH - Supraoptic Nucleus/cytology/metabolism/physiology MH - Vasopressins/blood/*metabolism MH - Water-Electrolyte Balance/physiology MH - Water-Electrolyte Imbalance/physiopathology PMC - PMC6741117 EDAT- 2003/05/24 05:00 MHDA- 2003/06/26 05:00 PMCR- 2003/11/15 CRDT- 2003/05/24 05:00 PHST- 2003/05/24 05:00 [pubmed] PHST- 2003/06/26 05:00 [medline] PHST- 2003/05/24 05:00 [entrez] PHST- 2003/11/15 00:00 [pmc-release] AID - 23/10/4261 [pii] AID - 10.1523/JNEUROSCI.23-10-04261.2003 [doi] PST - ppublish SO - J Neurosci. 2003 May 15;23(10):4261-9. doi: 10.1523/JNEUROSCI.23-10-04261.2003.