The medial septum acts through the medial preoptic area for thermoregulation and works with it for sleep regulation.

The chronic changes in sleep-wakefulness (S-W), body temperature (Tb), locomotor activity (LMA) and thermal preference were studied in male Wistar rats after the destruction of neurons in both the medial preoptic area (mPOA) and the medial septum (MS) by intracerebral injection of N-methyl-D-aspartic acid. An increase in the Tb, and a preference for higher ambient temperature (Tamb) of 30 degrees C were observed after the combined lesion of the mPOA and the MS. Similar changes were reported to occur after the lesion that was restricted to the mPOA. But these alterations were in contrast to the decrease in Tb and preference for lower Tamb, observed after the MS lesion. The thermostat of the brain would have been reset at a higher level after the combined lesion, as there was an increase in Tb, along with a preference for a higher Tamb, and an increase in LMA. There was a reduction in the frequency and the duration of the slow wave sleep (SWS) episodes, and a reduction in the frequency of the paradoxical sleep (PS) episodes after the combined lesion. The destruction of the MS neurons was probably responsible for the reduction in the frequency of SWS, whereas the loss of mPOA neurons was responsible for the decrease in the duration of SWS and frequency of PS. It can be suggested that the MS exerts its influence on thermoregulation through the mPOA. However, the MS and the mPOA seem to play independent, but complementary roles in sleep promotion.

Sleep changes during chronic cold exposure showed that the homeostatic requirement of sleep is reduced in the medial preoptic area lesioned rats.

The effects of chronic exposure to a mildly cold ambient temperature (T(a)) of 18 degrees C on sleep wakefulness (S-W) and brain temperature (T(br)) were studied in the medial preoptic area (mPOA) lesioned male Wistar rats. Electroencephalogram (EEG), electrooculogram (EOG) and electromyogram (EMG) electrodes were chronically implanted to assess S-W, and a thermocouple above the dura to record the T(br). After three recordings (24 h each) of S-W and T(br) at 24 degrees C, N-methyl D-aspartic acid (NMDA) was intracerebrally injected to produce bilateral destruction of neurons in the mPOA. There was decreased sleep and increased T(br) even four weeks after the mPOA lesion. T(a) of the environmental chamber was then reduced to 18 degrees C, and the S-W and T(br) were again recorded for 24 h each on the 1st, 7th, 14th, 21st, and on 28th days of continuous exposure to the mild cold T(a). Exposure to the cold produced further decrease in sleep and increase in the T(br). However, sleep came back to the pre-exposure level by the 14th day. An increase in the duration of sleep episodes was responsible for the restoration of sleep during chronic cold exposure. The study showed that the requirement of sleep was reset at a lower level in the mPOA lesioned rats. The mPOA lesion affected the sleep maintenance and sleep initiation, though the latter became evident only during chronic cold exposure. The magnitude of the acute changes in T(br) and S-W were less in the lesioned rats, as compared to those observed in the normal rats exposed to similar cold T(a). On the basis of these observations, it could be proposed that the mPOA plays some role in cold induced changes in thermoregulation and sleep regulation. The T(br) remained elevated throughout the period of cold exposure. Resetting of the T(br), at a higher level may be part of the homeostatic readjustment to restore sleep.

Effects of entorhinal cortex lesions on memory in different tasks

Lesions of the entorhinal cortex produce retrograde memory impairment in both animals and humans. Here we report the effects of bilateral entorhinal cortex lesions caused by the stereotaxic infusion of N-methyl-D-aspartate (NMDA) in rats at two different moments, before or after the training session, on memory of different tasks: two-way shuttle avoidance, inhibitory avoidance and habituation to an open field. Pre-or post-training entorhinal cortex lesions caused an impairment of performance in the shuttle avoidance task, which agrees with the previously described role of this area in the processing of memories acquired in sucessive sessions. In the inhibitory avoidance task, only the post-training lesions had an effect (amnesia). No effect was observed on the open field task. The findings suggest that the role of the entorhinal cortex in memory processing is task-dependent, perhaps related to the complexity of each task.