Mice deficient in oxytocin manifest increased saline consumption followingovernight fluid deprivation

Citation
Ja. Amico et al., Mice deficient in oxytocin manifest increased saline consumption followingovernight fluid deprivation, AM J P-REG, 281(5), 2001, pp. R1368-R1373
Citations number
22
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
281
Issue
5
Year of publication
2001
Pages
R1368 - R1373
Database
ISI
SICI code
0363-6119(200111)281:5<R1368:MDIOMI>2.0.ZU;2-A
Abstract
Male mice (9-13 mo of age) in which the gene for oxytocin (OT) had been del eted (OT -/-) were administered 0.5 M sodium chloride (NaCl) solution or ta p water as a two-bottle choice test following overnight fluid deprivation ( 1600 to 1000 the following day). Compared with wild-type cohorts (OT +/+), OT-deficient mice ingested sevenfold greater amounts of saline in the first hour following reintroduction of fluids, P< 0.001, and fourfold greater am ounts at the end of 6 h, P< 0.02. No significant difference in total water ingested was noted between the two genotypes at the end of either 1 or 6 h. If food deprivation accompanied the overnight fluid deprivation and food w as reintroduced 1 h after the reintroduction of both water and saline, OT - /- mice still ingested greater amounts of saline, but not water, than OT +/ + mice at both 1 h, P< 0.001, and 6 h, P< 0.02. No differences were noted b etween genotypes in the daily intake of 0.5 M NaCl solution or water during a 3-day observation period before the overnight fluid deprivation. The vol ume of saline consumed in each 24-h observation period represented about on e-tenth of the total fluids ingested in each genotype. We conclude that OT -/- mice display an enhanced salt appetite compared with OT -/- mice when f luid deprived overnight. The salt appetite was only apparent in the presenc e of a perturbation such as fluid deprivation, which predisposes the animal to moderate hypovolemia. The observations support an inhibitory role for O T in the control of sodium appetite in mice.