[Modeling of chronic sleep restriction for translational studies].

Objective: To develop of a chronic sleep restriction model in rats by repeated sleep deprivation using an orbital shaker and to determine whether this model leads to disturbances in sleep homeostatic mechanisms.

Material And Methods: Male Wistar rats (7-8 months old) underwent sleep restriction for five consecutive days: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Polysomnograms were recorded telemetrically throughout the day before sleep restriction (baseline), on the 1st, 3rd, 5th day of sleep restriction and 2 days after the end of sleep restriction (recovery period).

[Age-related differences in sleep disturbances in rat models of preclinical Parkinson's disease].

Objective: To describe the changes in temporal characteristics of sleep-wake cycle, which can serve as non-motor manifestations of an early stage of Parkinson's disease (PD), using the model of preclinical PD in rats of two age groups.

Material And Methods: A prolonged (up to 21 days) model of preclinical PD in middle-aged (7-8 month) and aged (19-20 month) rats was created. The model was based on cumulative inhibition of proteasomal system of the brain caused by intranasal administration of lactacystin, a specific proteasome inhibitor.

[Changes in characteristics of sleep-wake cycle and motor activity at the preclinical stage of Parkinson's disease in old rats].

Aim: To assess the changes in temporal characteristics and total motor activity (MA) during the sleep-wake cycle in old rats in the model of the preclinical stage of Parkinson's disease (PD).

Material And Methods: Progressing inhibition of proteasome system and prolonged (up to the 21st day) development of the preclinical stage of PD in 19-20-month Wistar rats was caused by the specific proteasomal inhibitor lactacystin administered twice with a week interval. Telemetric monitoring of sleep-wake cycle was performed along with the video recording of MA.

Impairment of non-associative learning in a rat experimental model of preclinical stage of Parkinson's disease.

An experimental model of the preclinical stage of Parkinson's disease was induced by double intranasal administration of the proteasome inhibitor lactacystin. The results demonstrated signs of cognitive impairments expressed as impaired non-associative learning. This was related to degeneration of one-third of dopaminergic neurons in the ventral tegmental area of the midbrain and their axons in the dorsolateral prefrontal cortex.

[SLOW-WAVE SLEEP AND MOLECULAR CHAPERONES].

From ancient times the mankind has been interested in a topical issue: why is it necessary to spend about one-third of human life for sleep? This review considers the main data on the key function of slow-wave sleep (SWS) and the molecular mechanisms of its regulation; the basic conclusions are presented below as a summary and hypotheses. 1. SWS has an energy-conserving function developed simultaneously with the evolution of tachimetabolism and endothermy/homoiothermy.

[Role of adenosine A(2A) receptors of preoptical area in realization of somnogenic effect of protein 70 kDa in pigeons].

In representatives of class of birds (pigeons Columba livia) using electrophysiological methods for the first time there was performed analysis of effects of microinjections into the hypothalamic ventrolateral preoptical area (VLPA) of antagonists of the adenosine A(2A) type receptors on the sleep-wale cycle under natural conditions and on realization of somnogenic effect of Heat shock protein 70 kDa (Hsp70). The following has been established: 1) microinjections of adenosine A(2A) receptors antagonist (8-(3-Chlorostyryl) caffeine (ChC)) into VLPA at the beginning of inactive phase of the 24-h period dose-dependently increase wakefulness and suppress sleep; 2) microinjections of Hsp70 into VLPA produce somnogenic effect manifested as an increase of the total time of slow sleep (SS) and enhancement of mechanisms of initiation and maintenance of SS; 3) block of adenosine A(2A) receptors by ChC suppresses the Hsp70-induced SS. The obtained data indicate participation of adenosine A(2A) receptors located in VLPA in modulation of the sleep-wake cycle under natural conditions and in realization of somnogenic effect of Hsp70 in pigeons.

Microinjection of 70-kDal heat shock protein into the oral reticular nucleus of the pons suppresses rapid eye movement sleep in pigeons.

Previous studies have demonstrated that increases in the duration of slow-wave sleep and decreases in somatovisceral measures in response to microinjections of 70-kDal heat shock protein (Hsp70) into the third ventricle in pigeons may be due to activation of GABAA receptors in the preoptic area of the hypothalamus. With the aim of identifying the transmitter mechanisms whose activation is temporally (2-3 h) linked with suppression of rapid eye movement sleep, the present studies were based on injection of Hsp70 into the oral reticular pontine nucleus (nucleus reticularis pontis oralis, NRPO), whose cholinergic neurons are critical for generating rapid eye movement sleep. Hsp70 was found to induce earlier (within the first 2 h) decreases in the number of episodes and the total duration of rapid eye movement sleep, with decreases in electroencephalogram (EEG) spectral power in the range 9-14 Hz, the level of muscle contractile activity, and brain temperature.

Role of the cholinergic mechanisms of the ventrolateral preoptic area of the hypothalamus in regulating the state of sleep and waking in pigeons.

Maintenance of waking in pigeons was found to be linked with the mechanisms of activation of muscarinic (M-) cholinergic receptors of the ventrolateral preoptic area of the hypothalamus. "Muscarinic" waking was characterized by an increase in the power of the EEG spectrum at 0.75-12 Hz and an increase in brain temperature.