Proinflammatory cytokines, including interleukin-1 beta and tumor necrosis
factor-alpha are involved in physiological sleep regulation. Interleukin (I
L)-13 and transforming growth factor (TGF)-beta 1 are anti-inflammatory cyt
okines that inhibit proinflammatory cytokines by several mechanisms. Theref
ore, we hypothesized that IL-13 and TGF-beta 1 could attenuate sleep in rab
bits. Three doses of IL-13 (8, 40, and 200 ng) and TGF-beta 1 (40, 100, and
200 ng) were injected intracerebroventricularly 3 h after the beginning of
the light period. In addition, one dose of IL-13 (200 ng) and one dose of
TGF-beta 1 (200 ng) were injected at dark onset. The two higher doses of IL
-13 and the highest dose of TGF-beta 1 significantly inhibited spontanenous
non-rapid eye movement sleep (NREMS) when they were given in the light per
iod. IL-13 also inhibited NREMS after dark onset administration; however, t
he inhibitory effect was less potent than that observed after light period
administration. The 40-ng dose of IL-13 inhibited REMS duration during the
dark period. TGF-beta 1 administered at dark onset had no effect on sleep.
These data provide additional evidence for the hypothesis that a brain cyto
kine network is involved in regulation of physiological sleep.