Osmotic Regulation of Estrogen Receptor-β in Rat Vasopressin and Oxytocin Neurons

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Abstract
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)-β. In contrast, only ∼7.5% of oxytocin (OT) MNCs express ER-β. We examined the osmotic regulation of ER-β mRNA expression in MNCs using quantitativein situhybridization 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-β mRNA expression in MNCs (p< 0.05). Thus, the expression of ER-β 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-β in MNCs. Immunocytochemistry demonstrated that the decrease in ER-β mRNA was translated into depletion of receptor protein content in hyper-osmotic animals. Numerous MNCs were positive for ER-β in control animals, but they were virtually devoid of ER-β-immunoreactivity (IR) in hyper-osmotic animals. The osmotically induced decrease in ER-β expression was selective for MNCs because ER-β-IR remained unaltered in PVN parvocellular neurons. Plasma estradiol and testosterone were not correlated with ER-β mRNA expression after osmotic manipulation, suggesting that ER-β expression was not driven by ligand availability. Expression of FOS-IR in MNCs with attenuated ER-β-IR, and the absence of FOS-IR in parvocellular neurons that retain ER-β-IR suggest a role for neuronal activation in the regulation of ER-β expression in MNCs. Thus, osmotic modulation of ER-β expression in MNCs may augment or attenuate an inhibitory effect of gonadal steroids on VP release.