Effects of factors inducing diffuse damage to brain tissue on sleep structure in laboratory rats.

Chronic experiments on laboratory rats with implanted electrodes for recording neocortical and hippocampal EEG and cervical muscle electromyogram traces were performed to study the effects of strong treatments inducing diffuse damage to brain tissue on subsequent sleep. Four different experimental models were used: one "chronic" (generalized cerebral ischemia induced by permanent occlusion of one of the common carotid arteries) and three "acute" (hypoxic hypoxia, hypoglycemia, and "penicillin" epilepsy). Sleep recordings were made in freely moving animals either day-round (in the "chronic" model) or daily for 3 h ("acute" models). In all models, traces showed significant increases in the mean total duration of paradoxical sleep, reaching a peak 1-3 days after treatment. The subsequent dynamics depended on the treatment used: in the "acute" models, the duration of paradoxical sleep returned to control levels in 5-6 days, while in the "chronic" model, this occurred at 40-45 days after the beginning of treatment. The sharp increases in the durations of paradoxical sleep after use of strong treatments inducing damage to brain tissue can be regarded as supporting the suggestion that there is an increase in neuronal recovery processes during paradoxical sleep.

[Effect of the exposure to factors inducing diffuse damage of cerebral tissue on sleep structure in laboratory rats].

Effects of strong stress inducing diffuse damage of the brain tissue on subsequent sleep were studied in rats preliminary implanted with chronic electrodes for the neocortical and hippocampal EEG as well as EMG of the neck muscles. An acute and three chronic experimental models were used: general cerebral ischemia induced by a permanent unilateral occlusion of the common carotid artery, hypoxic hypoxia, hypoglycemia, and "penicillinium" epilepsy. Polysomnographic recording was performed either continuously within 24 hrs (in case of the chronic stress model) or 3 hrs daily: from 09 to 12 a.m. (for three acute stress models). In all the models, a significant increase in the paradoxical sleep (PS) percentage was found which reached its maximum within 1-3 days since stress exposure. The following changes were found to be dependent upon the character of the stress factor. In acute stress models, the PS percentage returned to the baseline level within 5-6 days. In the chronic model, the PS percentage returned to baseline level on the 40-45th day after the day of occlusion. The sharp increase in the PS percentage following the exposure to stress factors inducing cerebral tissue damage corroborate the hypothesis of an increase in neural tissue restitution processes during PS periods.

[Increase in duration of paradoxical sleep after carotid occlusion in rats]. / Uvelichenie prodolzhitel'nosti paradoksal'noi fazy sna u krys, perezhivshikh okkliuziiu sonnoi arterii.

Nonlinear rats, which survived after occlusion of one or two common carotid arteries (N = 30, about 30% survived) were examined. Sham-operated animals formed a control group. In animals with ischemia, the total sleep duration in a three-hour period was substantially increased as compared to control group at the expense of a substantial growth (8-9 times) of paradoxical sleep (PS) phase. In the animals with ischemia, a sharp increase in PS was observed on the first postoperation day, and then PS gradually decreased from the first to the fortieth days. The results suggest the PS involvement in the brain intrinsic reparation functions.

[EEG of the interstimulus intervals during habituation of auditory evoked potentials in depressive moods]. / EEG mezhstimul'nykh intervalov v protsesse privykaniia slukhovykh vyzvannykh potentsialov pri depressivnykh nastroeniiakh.

Averaging of EEG of interstimulus intervals in the process of study of habituation of auditory evoked potentials (EPs) in healthy subjects and patients with endogenous depression, revealed a rhythmic wave process (RWP) especially expressed in patients. RWP appeared and became stronger in successive averaging of 10 realizations completing each of four series of 30 clicks; often (especially in depressive patients) it was manifest in averaging of all 120 realizations with an amplitude comparable with that of main EPs components and even greater. A significant correlation was found of RWP parameters with characteristics of melancholic mood in both subgroups. It is suggested that RWP appears as a result of regular changes of EEG background during multiple stimuli repetition in connection with increased "slow" habituation and in a special manifestation of perceptive defence during depression including mechanisms of active isolation from external world.

[Habituation of auditory evoked potentials and emotional state]. / Privykanie slukhovykh vyzvannykh potentsialov i émotsional'noe sostoianie.

"Fast" and "slow" habituation of N1 and N1-P2 components of auditory evoked potentials was studied in healthy subjects and in depressed patients. In patients, initially more low amplitudes of N1 and N1-P2 were revealed, as well as slowing down of habituation in the beginning of stimuli series and acceleration to its end (in healthy people--the greatest habituation in the initial part of the series and amplitude increase at its end), the absence of power effect in the component N1 at reaching, in the process of habituation, of the same minimum parameters as in healthy subjects. This points to weakening of dishabituation process parallel with well expressed "slow" habituation in patients and allows to suggest at expressed negative emotions a deficit of attention processes as a result of "internal abstraction".

[Changes in the wave composition of evoked potentials during treatment of endogenous depression]. / Izmenenie volnovogo sostava vyzvannykh potentsialov pri lechenii éndogennoi depressii.

Evoked potentials (EPs) were studied in patients with endogenic depression prior to and during the therapy. It was found that a reduction in the maximum amplitude of EPs reflecting the initial severity of depression could not serve as an indicator of its time-course in the treatment by tricyclic antidepressants. In contrast, the newly identified electrophysiological sign of endogenic depression, a number of EP waves, shifted toward normalization in the process of the treatment parallelled by a decrease in the severity of the depressive syndrome.