title: Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat.
abstract: Hyperosmotic intravenous infusions of NaCl are more potent for inducing drinking and vasopressin (AVP) secretion than equally osmotic solutions of glucose or urea. The fact that all three solutes increased cerebrospinal fluid osmolality and sodium concentration led the investigators to conclude that critical sodium receptors or osmoreceptors for stimulating drinking and AVP secretion were outside the blood-brain barrier (BBB) in the circumventricular organs (CVOs). We tested an obvious prediction of this hypothesis: that all three solutes should increase c-Fos-like immunoreactivity (Fos-ir) inside the BBB, but that only NaCl should increase Fos-ir in the CVOs. We gave intravenous infusions of 3.0 Osm/l NaCl, glucose, or urea to rats for 11 or 22 min at 0.14 ml/min and perfused the rats for assay of Fos-ir at 90 min. Controls received isotonic NaCl at the same volume. Drinking latency was measured, but water was then removed. Drinking consistently occurred with short latency during hyperosmotic NaCl infusions only. Fos-ir in the forebrain CVOs, the subfornical organ, and organum vasculosum laminae terminalis was consistently elevated only by hyperosmotic NaCl. However, all three hyperosmotic solutes potently stimulated Fos-ir in the supraoptic and paraventricular nuclei of the hypothalamus inside the BBB. Hyperosmotic NaCl greatly elevated Fos-ir in the area postrema, but even glucose and urea caused moderate elevations that may be related to volume expansion rather than osmolality. The data provide strong support for the conclusion that the osmoreceptors controlling drinking are located in the CVOs.
authors.affiliation: Department of Psychology, University of Washington, Box 351525, Seattle, WA 98195-1525, USA.
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Ho
authors.forename: Dannielle K
authors.initials: DK
authors.lastname: Zierath
authors.forename: Anna V
authors.initials: AV
authors.lastname: Savos
authors.forename: Dominic J
authors.initials: DJ
authors.lastname: Femiano
authors.forename: John E
authors.initials: JE
authors.lastname: Bassett
authors.forename: Michael J
authors.initials: MJ
authors.lastname: McKinley
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Fitts
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier; D002552:Cerebral Ventricles; D004327:Drinking Behavior / Q000187:drug effects*; D007031:Hypothalamus / Q000378:metabolism; D007150:Immunohistochemistry; D007262:Infusions, Intravenous; D008297:Male; D009994:Osmolar Concentration; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D012462:Saline Solution, Hypertonic