Hypo-osmolarity stimulates and high sodium concentration inhibits thyrotropin-releasing hormone secretion from rat hypothalamus

• Published in: Neuroscience Vol. 88; no. 4; pp. 1299 - 1306
• Main Authors: Nikodémová, M, Greer, M.A, Štrbák, C
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01-02-1999; Elsevier
• Subjects: Animals; Biological and medical sciences; Choline - administration & dosage; Choline - pharmacology; Culture Media - chemistry; Culture Media - pharmacology; Fundamental and applied biological sciences. Psychology; Glucose - administration & dosage; Glucose - pharmacology; Hormones and neuropeptides. Regulation; hypothalamus; Hypothalamus - metabolism; Hypothalamus. Hypophysis. Epiphysis. Urophysis; Male; median eminence; Na + ions; Osmolar Concentration; osmotic regulation; paraventricular nucleus; Rats; Rats, Wistar; secretion; Sodium - metabolism; Sodium Chloride - administration & dosage; Sodium Chloride - pharmacology; Thyrotropin-Releasing Hormone - antagonists & inhibitors; Thyrotropin-Releasing Hormone - metabolism; TRH; Vertebrates: endocrinology; osmotic regulation; SON, supraoptic nucleus; TRH, thyrotropin-releasing hormone; secretion; ME, median eminence; HEPES, N-2-hydroxyethylpiperazine- N′-2-ethanesulphonic acid; PVN, paraventricular nucleus; median eminence; Na + ions; TRH; hypothalamus; paraventricular nucleus; Rat; Secretion; Rodentia; Central nervous system; Osmoregulation; Hypothalamus; Paraventricular nucleus; Hypothalamic hormone; Vertebrata; Thyrotropin releasing hormone; Mammalia; Sodium; Hormone releasing factor; Brain (vertebrata)
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(98)00279-6

The hypothalamic paraventricular nucleus, representing cell bodies in which thyrotropin-releasing hormone is synthesized, and the median eminence, representing nerve terminals, were incubated
in vitro. Various hypo- and hyperosmotic solutions were tested to determine osmotic sensitivity of thyrotropin-releasing hormone secretion. High KCl (56
mM) causing membrane depolarization was used as a non-specific control stimulus to induce thyrotropin-releasing hormone secretion. A 30% decrease of medium osmolarity (from 288 to 202
mOsmol/l) increased thyrotropin-releasing hormone secretion from both the paraventricular nucleus and median eminence. A 30% decrease of medium NaCl content by its replacement with choline chloride did not affect basal thyrotropin-releasing hormone secretion. Increasing medium osmolarity with biologically inactive
l-glucose did not affect basal or KCl-induced thyrotropin-releasing hormone secretion from either structure. Medium made hyperosmotic (350–450
mOsmol/l) by increasing the NaCl concentration resulted in a dose-dependent decrease of basal thyrotropin-releasing hormone secretion and abolished KCl-induced thyrotropin-releasing hormone secretion. If an osmotically equivalent amount of choline chloride was substituted for NaCl, there was no effect on thyrotropin-releasing hormone secretion, indicating a specific action of Na
+.
This study indicates a specific sensitivity to high concentrations of Na
+ ions of both thyrotropin-releasing hormone-producing parvocellular paraventricular neurons and of thyrotropin-releasing hormone-containing nerve terminals in the median eminence.