Osmotic regulation of estrogen receptor-beta in rat vasopressin and oxytocin neurons

• Published in: The Journal of neuroscience 2003-05, Vol.23 (10), p.4261-4269
• Main Authors: Somponpun, Suwit J, Sladek, Celia D
• Format: Article
• Language: English
• Subjects: Animals; Behavioral/Systems/Cognitive; Blood Volume - physiology; Body Weight - physiology; Estrogen Receptor beta; Hematocrit; Hormones - blood; Hormones - physiology; Hypernatremia - physiopathology; Hyponatremia - physiopathology; Male; Neurons - cytology; Neurons - metabolism; Osmolar Concentration; Osmotic Pressure; Oxytocin - blood; Oxytocin - metabolism; Paraventricular Hypothalamic Nucleus - cytology; Paraventricular Hypothalamic Nucleus - metabolism; Paraventricular Hypothalamic Nucleus - physiology; Rats; Rats, Sprague-Dawley; Receptors, Estrogen - biosynthesis; Receptors, Estrogen - genetics; Receptors, Estrogen - metabolism; Sodium Chloride - metabolism; Supraoptic Nucleus - cytology; Supraoptic Nucleus - metabolism; Supraoptic Nucleus - physiology; Vasopressins - blood; Vasopressins - metabolism; Water-Electrolyte Balance - physiology; Water-Electrolyte Imbalance - physiopathology
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/jneurosci.23-10-04261.2003

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.