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AJP - Regulatory, Integrative and Comparative Physiology, Vol 259, Issue 4 741-R744, Copyright © 1990 by American Physiological Society
ARTICLES |
P. G. Osborne, J. R. Blair-West, D. A. Denton, M. McBurnie, E. Tarjan, R. M. Williams and R. S. Weisinger
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia.
BALB/c mice were allowed free access to water, food, and 0.3 M NaCl. Intracerebroventricular infusion of 0.7 M mannitol in artificial cerebrospinal fluid (CSF) was used to reduce CSF sodium concentration. The infusion was made at 24 microliters/day, which was similar on a body weight basis to the rate that evoked a large increase in sodium appetite in sheep. Reduction of CSF sodium concentration did not increase the voluntary sodium intake of sodium-replete mice or furosemide-treated, sodium-depleted mice. Thus, in contrast to findings in sheep and cattle and similar to the findings in the laboratory rat and wild rabbits, changes in cerebral sodium concentration are apparently not involved in the sodium appetite of mice.
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