EXPOSURE TO HEAT RESTORES SLEEP IN CATS WITH PREOPTIC ANTERIOR HYPOTHALAMIC CELL LOSS

Evidence suggests that thermosensitive neurons of the preoptic/anterior hypothalamus (POAH) influence sleep- and arousal-regulating mechanisms. We examined the effects of POAH cell loss, produced by microinjection of neurotoxin (N-methyl-DL-aspartic acid), on sleep and thermoregulation in cats. Cats with bilateral POAH cell loss did not defend their body temperatures in the heat as effectively as normals, and did not initiate panting until brain temperatures rose to abnormally high levels. During 14 h polygraphic recordings of sleep-waking state conducted at an ambient temperature (T(a)) of 23-degrees-C, POAH-damaged cats exhibited reduced sleep. Amounts of deep slow-wave sleep (SWS2) were significantly less than prelesion values through 7 weeks postlesion; significant REM sleep deficits persisted for 5 weeks. However, these sleep disturbances were dramatically attenuated when cats were exposed to high T(a)S. During 6 h recordings at T(a)S of 13, 23, or 33-degrees-C, total sleep time was greatest at 33-degrees-C at both 2 and 4 weeks postlesion. At 4 weeks, amounts of SWS2 at 33-degrees-C were similar to maximal prelesion values. Increased sleep at 33-degrees-C was associated with elevated brain temperatures. The finding that, after POAH damage, abnormally high brain temperatures were required to elicit both panting and normal amounts of SWS suggests that impaired hypothalamic sensitivity to heat was responsible for both deficits. These results support the hypothesis that thermosensitive neurons participate in the tonic regulation of sleep and arousal.