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Volume 17, Number 15,
Issue of August 1, 1997
pp. 5949-5955
Copyright ©1997 Society for Neuroscience
Mice Lacking the TNF 55 kDa Receptor Fail to Sleep More After
TNF Treatment
Received Feb. 5, 1997; revised April 28, 1997; accepted May 12, 1997.
Jidong Fang ,
Ying Wang , and
James M. Krueger
Department of Physiology and Biophysics, University of Tennessee,
Memphis, Tennessee 38163
Tumor necrosis factor (TNF) is a well characterized
sleep-regulatory substance. To study receptor mechanisms for the
sleep-promoting effects of TNF, sleep patterns were determined in
control and TNF 55 kDa receptor knock-out (TNFR-KO) mice with a B6 × 129 background after intraperitoneal injections of saline or murine
TNF . The TNFR-KO mice had significantly less baseline sleep than the
controls. TNF dose-dependently increased non-rapid eye movement
sleep (NREMS) in the controls but did not influence sleep in TNFR-KO
mice. Although TNFR-KO mice failed to respond to TNF, they had an
increase in NREMS and a decrease in rapid eye movement sleep after
interleukin-1 treatment. These results indicate that TNF affects
sleep via the 55 kDa receptor and provide further evidence that TNF
is involved in physiological sleep regulation. Current results also extend the list of species to mice in which TNF and interleukin-1 are somnogenic.
Key words:
knock-out mice;
REM sleep;
slow-wave sleep;
TNF receptor;
EEG slow-wave activity;
interleukin-1
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