EARLY POSTNATAL DYSFUNCTIONING OF THE BRAIN MUSCARINIC CHOLINERGIC SYSTEM AND THE DISORDERS OF FEAR-MOTIVATED LEARNING AND MEMORY.

The aim of the study was to investigate the early postnatal dysfunctioning of the brain muscarinic cholinergic system as a major factor in the development of cognitive disorders similar with somewhat is noted in animal models of depression and in patients with Major Depressive Disease. The present study examined the processes of learning and long-term retention of information obtained in the two important tasks of non-declarative memory - active avoidance, motivated by foot shock-induced fear, and the elevated plus-maze, based on the natural fear.Experiments were carried out on male white wild rats (n=60).

ACQUISITION AND CONSOLIDATION OF TWO-WAY ACTIVE AVOIDANCE IN THE HIGH IMMOBILIZATION "DEPRESSIVE" RATS.

Present study investigated possible changes in acquisition and consolidation of associative memory in high immobilization "depressive" and low immobilization "non-depressive" rats. Question is very topical because understanding the character of learning and memory disturbances, one of symptoms of major depressive disease, is very significant for more intimate definition of the pathophysiology of major depressive disorder and appropriate searching the ways of its correction. Selection of rats according to the level of immobilization was made by means of forced swim test.

CHARACTER OF THE CHANGES IN FEAR MOTIVATED DECLARATIVE MEMORY IN THE HIGH IMMOBILIZATION "DEPRESSIVE" RATS.

Present study investigated possible differences in the learning and memory of declarative memory task in rats selected according to the differences in immobilization response that is in high immobilization "depressive" and low immobilization "non-depressive" rats. Understanding the character of learning and memory disturbances in basal conditions of animal models of depression is still very topical for more intimate definition of the pathophysiology of major depressive disorder and appropriate searching the ways of its correction. Experiments were carried out on the adult white wild rats (with the weight 200-250 g, n=20).

HYPOTHALAMIC OREXINE SYSTEM ACCELERATES REGULATION OF SLEEP HOMEOSTASIS AND SLEEP-WAKEFULNESS CYCLE RECOVERY FROM BARBITURATE ANESTHESIA-INDUCED ARTIFICIAL SLEEP.

The work was aimed for the ascertainment of following question - whether Orexin-containing neurons of dorsal and lateral hypothalamus and brain Orexinergic system in general are those cellular targets which can accelerate recovery of disturbed sleep homeostasis and restoration of sleep-wakefulness cycle behavioral states from barbiturate anesthesia-induced artificial sleep. Investigation was carried out on 18 wild type white rats (weight 200-250gr). Different doses of Nembutal Sodium were used for the initiation of deep anesthesia.

Influence of serial electrical stimulations of perifornical and posterior hypothalamic orexin-containing neurons on regulation of sleep homeostasis and sleep-wakefulness cycle recovery from experimental comatose state and anesthesia-induced deep sleep.

The work was aimed for the ascertainment of following question - whether Orexin-containing neurons of dorsal and lateral hypothalamic, and brain Orexinergic system in general, are those cellular targets which can speed up recovery of disturbed sleep homeostasis and accelerate restoration of sleep-wakefulness cycle phases during some pathological conditions - experimental comatose state and/or deep anesthesia-induced sleep. Study was carried out on white rats. Modeling of experimental comatose state was made by midbrain cytotoxic lesions at intra-collicular level.