Effect of Lateral Preoptic Area Lesion on Sleep Wakefulness and Thermoregulation In Cold Acclimatized Rats.

Hypothalamic temperature (Thy) alteration is one of the important stimuli that brings about thermoregulatory measures including the changes in wakefulness and muscular activity. The role of the lateral preoptic area (lPOA) in thermoregulation and sleep is well documented. But it is not known whether the integrity of the lPOA is essential for bringing about the changes in sleep-wakefulness (S-W) and thermoregulation in cold ambient temperature (Ta). Neurotoxic lesion of the lPOA resulted in an increase in wake period and core body temperature (Tb) and no change in Thy. Unlike, normal animals, as reported earlier, there was further increase in Tb of the lPOA lesioned rats on acute cold exposure, but the Thy remained unaltered throughout the 28 days of continued cold exposure. The findings demonstrate that the lPOA lesioned rats have lost the ability to reset Thy which may be necessary for thermoregulation during cold exposure. Moreover, increased wake period lasted only 7 days in lesioned, compared to 14 days in normal animals. Less efficient restoration of Tb, and less prolonged wake period during continued cold exposure, are probably the result of the inability of the lPOA lesioned rats to lower Thy, which is necessary to bring about the thermoregulatory measures.

Hypothalamic temperature: A key regulator in homeostatic restoration of sleep during chronic cold exposure in rats.

Exposure to cold ambient temperature (Ta) affects sleep-wake (S-W) state. The vigilance states on the other hand influence thermal status of the animals. Simultaneous recording of body temperature (Tb) with S-W is crucial to understand the homeostatic relationship between the two. In the present study we recorded both Tb and hypothalamic temperature (Thy) along with S-W, during acute and chronic exposure to mild cold (Ta). Electrooculogram (EOG), electroencephalogram (EEG) and electromyogram (EMG) electrodes were chronically implanted in rats to assess S-W. A thermocouple, near the preoptic area, and radio transmitter in the peritoneum, were implanted, to record Thy and Tb respectively. After three days of baseline recordings of S-W, Thy and Tb at Ta of 26°C, the rats were exposed to mild cold Ta (18°C) for 28 days. All the parameters were recorded during cold exposure and also for five days after the termination of cold exposure. On the first day of cold exposure there was a decrease in slow wave sleep and paradoxical sleep, but they were restored by the 21st day of continued exposure. The Thy remained decreased throughout the cold exposure. Though the Tb showed a slight decrease on the first day of cold exposure, there was no appreciable change during the subsequent days. The Thy came back to near pre exposure level on termination of cod exposure. The decrease in Thy during mild cold exposure would have triggered cold defense mechanisms. Increase in wakefulness during acute cold exposure and non-shivering thermogenesis during chronic cold exposure are probably responsible for the maintenance of Tb. Decrease in Thy is probably the key trigger for initiating thermoregulatory measures to maintain Tb and homeostatic restoration of sleep.