Mice lacking the transient receptor vanilloid potential 1 channel display normal thirst responses and central Fos activation to hypernatremia.
Neurons of the organum vasculosum of the lamina terminalis (OVLT) are necessary for thirst and vasopressin secretion during hypersmolality in rodents. Recent evidence suggests the osmosensitivity of these neurons is mediated by a gene product encoding the transient receptor potential vanilloid-1 (TRPV1) channel. The purpose of the present study was to determine whether mice lacking the TRPV1 channel had blunted thirst responses and central Fos activation to acute and chronic hyperosmotic stimuli. Surprisingly, TRPV1-/- vs. wild-type mice ingested similar amounts of water after injection (0.5 ml sc) of 0.5 M NaCl and 1.0 M NaCl. Chronic increases in plasma osmolality produced by overnight water deprivation or sole access to a 2% NaCl solution for 48 h produced similar increases in water intake between wild-type and TRPV1-/- mice. There were no differences in cumulative water intakes in response to hypovolemia or isoproterenol. In addition, the number of Fos-positive cells along the lamina terminalis, including the OVLT, as well as the supraoptic nucleus and hypothalamic paraventricular nucleus, was similar between wild-type and TRPV1-/- mice after both acute and chronic osmotic stimulation. These findings indicate that TRPV1 channels are not necessary for osmotically driven thirst or central Fos activation, and thereby suggest that TRPV1 channels are not the primary ion channels that permit the brain to detect changes in plasma sodium concentration or osmolality.
Taylor
A Caitlynn
AC
Department of Physiology, University of Kentucky, Lexington, KY 40536, USA.
McCarthy
John J
JJ
Stocker
Sean D
SD
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D004232:Diuretics / Q000494:pharmacology; D004326:Drinking / Q000187:drug effects; D005665:Furosemide / Q000494:pharmacology; D005838:Genotype; D006400:Hematocrit; D006955:Hypernatremia / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009994:Osmolar Concentration; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism / Q000503:physiopathology; D010641:Phenotype; D011301:Preoptic Area / Q000378:metabolism / Q000503:physiopathology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage / Q000378:metabolism; D013495:Supraoptic Nucleus / Q000378:metabolism / Q000503:physiopathology; D050916:TRPV Cation Channels / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D013894:Thirst / Q000187:drug effects; D013997:Time Factors; D014882:Water-Electrolyte Balance / Q000187:drug effects
D000318:Adrenergic beta-Agonists; D001798:Blood Proteins; D004232:Diuretics; D016760:Proto-Oncogene Proteins c-fos; D012462:Saline Solution, Hypertonic; D050916:TRPV Cation Channels; C493921:TRPV1 protein, mouse; D005665:Furosemide; D007545:Isoproterenol