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M N Aliev

Publications and source records attributed to M N Aliev.

At least 19 recordsLinked to original sources
PubMed1994

[The role of lipid peroxidation in the pathogenesis of neuropathological syndromes and in experimental therapy].

Activated lipid peroxidation observed in brain homogenates in experimental choreoid hyperkinesis and bemegride epilepsy can be arrested by antioxidant pretreatment. The same is true for parkinsonian and "malignant locomotion" syndromes provoked by intrastriatal pro-oxidant (oxidized oleinic acid) microinjection and systemic administration of haloperidol. Experimental therapy of choreoid hyperkinesis with GABA-positive and dopamine-blocking drugs alone proved ineffective. The effect was achieved at combined application of antioxidant and GABA-positive drugs.

Animals↗
PubMed1986

[Antenatal prevention, using lithium oxybutyrate, of changes in the development of the rat brain caused by serum from schizophrenic patients].

It has been found that antenatal administration of schizophrenic patients' sera to rats has neuroembryotoxic effect on their progeny, decreasing the number of females in the brood, disturbing motor coordination and space perception in young male rats, slightly stimulating muscular force and motor activity, altering lateralization of the behaviour. Antenatal lithium hydroxybutyrate was shown to prevent some of the serum effects.

Adult↗
PubMed1981

The stereotyped behavior syndrome: a new model and proposed therapy.

The stereotyped behavior syndrome was induced in rats through local impairment of inhibitory GABA-ergic mechanisms in both caudate nuclei by bilateral microinjection of tetanus toxin, penicillin, or picrotoxin into the rostral part of the caudate nucleus. Intraperitoneally injected haloperidol suppressed the syndrome; this effect was dose-dependent. The same effect on the tetanus toxin-induced stereotyped behavior was produced by GABA microinjected bilaterally into the rostral part of the caudate nucleus of unrestrained rats. It was found in this model of tetanus toxin-induced stereotyped behavior that lithium chloride and diazepam can suppress the syndrome. Combined application of lithium chloride, diazepam, and haloperidol in minimal effective doses resulted in a much more complete and longer-lasting suppression of the syndrome than the separate use of these drugs. This effect is attributed to the joint specific actions of the drugs on pathogenetically interrelated components of a hyperactive determinant structure that arises in the caudate nuclei after impairment of the GABA control and this is responsible for the stereotyped behavior syndrome.

Animals↗
PubMed1981

[Formation of a generator of pathologically enhanced excitation in the caudate nucleus in experimental parkinsonism].

Rats with the Parkinsonian syndrome induced by administering tetanus toxin to the rostral part of both the caudate nuclei manifest an increased electrical activity in this part. The increase is marked by the rise of the number of points where the neuronal activity is recordable, by a greater frequency of the background impulse activity of the neurons and by the appearance of the neurons with packet activity. The data obtained allow the conclusion that administration of tetanus toxin that disturbs the inhibition mechanisms including dopamine secretion results in the formation of the caudate nuclei of the generator of pathologically enhanced excitation which seems likely to form the neuropathophysiological basis of the Parkinsonian syndrome.

Animals↗
PubMed1979

[Experimental stereotypy caused by disorders of GABA-ergic mechanisms in the caudate nuclei].

The stereotypy was induced in rats by forming generators of pathologically intensified excitation (GPIE) on local disturbance of the inhibitory mechanisms in rostral portion of caudate nuclei, using bilateral injection of tetanus toxin. Microinjections of gamma-amino-butyric acid (GABA) into the area of the GPIE and systemic galoperidol administration inhibited the stereotypic behaviour of the animals. It is concluded that the formation of the GPIE may lie in the basis of stereotypy due to the disturbances in presynaptic link of the gamkergic system of caudate nuclei, dopaminergic neurons being an operant part of this GPIE.

Animals↗
PubMed1979

[Pathogenesis of stereotyped behavior].

The paper concerns the syndrome of stereotyped behaviour in rats induced by disturbance of inhibition in both caudate nuclei under influence of tetanus toxin, penicillin, and pirotoxin injected in these nuclei. Stereotyped behaviour could be inhibited by administration of GABA into the same brain area, as well as by a systemic administration of haloperidol, diazepam, aminalon, and lithium chloride. The conclusion is made that the disturbance of GABA-egric control in the caudate nucleus is a significant pathogenetic condition of the hyperactive neostriar dofaminergic apparatus, appearing due to disinhibition. Both links compose the pathogenetic basis of the syndrome of stereotyped behaviour.

Animals↗
PubMed1976

[Experimental neuropathological syndromes during the development of hyperactive determinant dispatch stations in the caudate nuclei].

Hyperactive determinant dispatch stations (DDS), representing generators of pathologically increased excitation, were created in the rostral part of both caudate nuclei in rats with the aid of tetanus toxin, which disturbed various kinds of inhibition. Formation of such DDS generators in the indicated structures induced stereotypes, impulsive convulsive movements and catalepsy.

Animals↗
PubMed1975

[Disorder of gamma-motor neuronal activity in experimental thyrotoxicosis].

The activity of gamma-motor neurons was studied in the anesthetized rats following per os administration of thyroidin for 3 weeks. In experimental thyrotoxicosis against the backgrounds of an increased amount of mute filaments isolated from the stem of the n. gastrocnemius there was an increase in the frequency of discharge of the flexors and extensors of the gamma-motor neurons. A high frequency not peculiar to that of intact animals was recorded in the flexors of the gamma-motor neurons of the animals receiving thyroidin.

Animals↗