Inhibition of tumor necrosis factor prevents warming-induced sleep
responses in rabbits.
Takahashi, Satoshi, and James M. Krueger.
Department of Physiology and Biophysics, University of Tennessee,
Memphis, TN 38163 USA
APStracts 3:0424R, 1996.
Tumor necrosis factor (TNF) is a key regulatory component of sleep. In
the present study, we determined the effects of
intracerebroventricular (icv) injection of a TNF inhibitor, a soluble
TNF receptor fragment (TNFRF), on sleep responses of rabbits during
and after exposure to mild increases in ambient temperature (Tamb).
Each rabbit (n=8) was recorded from under three conditions: a) normal
Tamb (21[circumflex]uC) with pyrogen-free saline (PFS) 50 [mu]l icv;
b) 27[circumflex]uC Tamb with PFS icv; and c) 27[circumflex]uC Tamb
with the TNFRF 50 [mu]g icv. When Tamb was increased to
27[circumflex]uC from 21[circumflex]uC, it was kept at that
temperature for 6 h after injection. The higher Tamb alone
significantly increased non-rapid-eye-movement sleep (NREMS),
decreased rapid-eye-movement sleep (REMS) and increased brain
temperature (Tbr) across the 23-h recording period.
Electroencephalogram (EEG) slow wave activity (SWA) was also
significantly enhanced during the 6-h warming period. In contrast,
all of the sleep responses associated with the higher Tamb were
absent if rabbits were pretreated with the TNFRF. The elevated Tbr
during the higher Tamb was not affected by the TNFRF. The present
results suggest that brain TNF is involved in the mild increases in
Tamb-induced sleep responses.
Received 19 July 1996; accepted in final form 4 November 1996.
APS Manuscript Number R421-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996