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|Title:||Effects of Environmental Temperature on Sleep and Waking in Normal Rats and Rats With Basal Forebrain Damage|
|Author(s):||Szymusiak, Ronald S.|
|Department / Program:||Psychology|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Abstract:||Damage to the basal forebrain (preoptic area and surrounding structures) causes hyposomnia and impairs body temperature regulation. Normal sleep is sensitive to thermal stress--animals spend the most time asleep at thermoneutral temperatures, and amounts of sleep decline in the heat and in the cold. Amounts of rapid-eye-movement (REM) sleep in normal rats vary within the thermoneutral zone defined by minimal metabolic rate--25 to 31(DEGREES)C--peaking toward the upper end of this zone (Szymusiak and Satinoff, Physiol. Behav. 26:687, 1981). Given the sensitivity of normal sleep to small changes in thermal stress, sleep disturbances produced by basal forebrain damage may, in part, be secondary to impaired thermoregulation.
Rats were hyposomniac after electrolytic basal forebrain ablations, but the sleep that remained was highly temperature-dependent. At 1-2 days postlesion, sleep was depressed at all environmental temperatures examined. However, during the subsequent 4-6 weeks, amounts of slow-wave sleep (SWS), REM sleep, total sleep time (TST), and the ratio of REM sleep time to TST (REM/TST) all improved significantly at thermoneutral temperatures. In contrast, at slightly higher or lower temperatures, these variables were as depressed one month after basal forebrain damage as they were at 5 days postlesion. REM/TST improved most rapidly, returning to control levels at thermoneutral temperatures within the first postlesion week. REM bout durations were severely depressed following basal forebrain damage, and this was the only sleep disturbance not attenuated at thermoneutral temperatures.
In summary, rats were hyposomniac after basal forebrain ablations, but the sleep that remained exhibited an exaggerated sensitivity to environmental temperature. As a result, most sleep disturbances were significantly attenuated at some temperatures but not at others. These results demonstrate the importance of controlling for possible thermoregulatory influences on sleep disturbances produced by brain damage.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1982.
|Date Available in IDEALS:||2014-12-15|