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K S Raevskiĭ

Publications and source records attributed to K S Raevskiĭ.

At least 91 records · Page 5Linked to original sources
PubMedDate not supplied

[Semax potentiates effects of D-amphetamine on the level of extracellular dopamine in the Sprague-Dawley rat striatum and on the locomotor activity of C57BL/6 mice].

The synthetic peptide semax (a fragment of ACTH 4-7 Pro-Gly-Pro) enhances the release of extracell dopamine (DA) induced by D-amphetamine (5 mg/kg) in the striatum of Spraig-Dowley (SD) rats and increases the locomotor activity stimulated by D-amphetamine (2 mg/kg) in C57/BL6 mice. The basal content of DA, 3,4-dihydroxyphenylacetic acid (DHPAA), and homovanillic acid (HVA) in dialysate of SD rats was 0.5-1.0, 996 +/- 25, and 761 +/- 37 pmole/ml, respectively (n = 7). D-amphetamine (5 mg/kg) induced a sharp increases in the DA level (up to 20 pmole/ml) 20-40 min after treatment and reduced the extracell DHPAA content to 30% of the basal level for a prolonged time (over the entire experimental period). Preliminary (20 min before D-amphetamine) administration of semax resulted in a greater peak of DA concentration (p < 0.05) and a more pronounced drop in DHPAA level (p < 0.01) as compared to the effects produced by the psychostimulant alone. In behavioral tests on C57/BL6 mice, D-amphetamine (2 mg/kg) increased the locomotor activity to a level of 182% (p < 0.01). Simultaneous introduction of semax (0.6 mg/kg) and D-amphetamine (2 mg/kg) led to a more pronounced increase in the locomotor activity of mice (261%, p < 0.01). It is suggested that the peptide modulates dopaminergic systems involved in the formation of the psychostimulant effect.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[The function of the peripheral adrenergic link under the action of neuroleptics in immobilization stress].

The morphofunctional state of different links of the sympathoadrenal system under the action of neuroleptics haloperidol and sulpiride was studied on the model of immobilization stress in rats. The drugs were shown to possess the effect of the pharmacological correction of hormone content in the adrenals and the level of the neuromediator activity of the adrenergic nerves at different stages of immobilization stress. The data obtained indicate the anti-stress action of the studied neuroleptics. The effect of sulpiride is noted both in the early (the stage of anxiety) and late (the stage of exhaustion) periods of immobilization. The action of haloperidol is mainly limited to the stage of anxiety.

Adrenal Medulla↗
PubMedDate not supplied

[Monoamine antagonism in relation to the direct effect of neuroleptics on the release of stimulating amino acid neuromediators].

In the experiments on the superfused synaptosomes of the rat brain cortex it was shown that both typical and atypical neuroleptics in the micromolar range of concentrations decrease K(+)-stimulated 3H-D-aspartate release. Serotonin (10(-5) M) and dopamine (10(-7) M) do not affect D-aspartate release. Serotonin abolishes the action of all typical neuroleptics studied (haloperidol, chlorpromazine, fluphenazine) and of sulpiride and clozapine, but not of carbidine. Dopamine antagonizes only the effect of atypical neuroleptics.

Animals↗
PubMedDate not supplied

[Comparative effect of the psychostimulants sidnocarb and fenamin on the tyrosine hydroxylase activity of the brain synaptosomes in rats].

A single administration of the psychostimulant sydnocarb activates tyrosine hydroxylase (TH) in synaptosomes of rat brain hypothalamus and striatum. The inhibitory effect of dopamine (DA) in synaptosomes of the striatum is potentiated. A single administration of amphetamine activates the response in synaptosomes of the hypothalamus and activates it in the striatum. Amphetamine does not exert any effect on the inhibitory effect of DA. Chronic administration of sydnocarb activates synaptosomal TH in the hypothalamus and inhibits it in the striatum. Fifteen minutes after the last injection of the two-week sydnocarb treatment the regulatory effect of DA in respect to tyrosine hydroxylation is considerably reduced. Thirty minutes after the concluding injection of the 2-week amphetamine treatment TH is found to be activated in the hypothalamus and inhibited in the striatum. Twenty-four hours after the treatment is completed the reverse relations are observed. The regulatory inhibitory effect of DA in respect to TH was significantly reduced in both versions of experiment.

Amphetamine↗
PubMedDate not supplied

[Effect of the atypical neuroleptics carbidine and sulpiride on dopamine biosynthesis in the synaptosomes of the nucleus accumbens septi in rats].

Neurochemical mechanisms of actions of atypical neuroleptics carbidine (a derivative of gamma-carboline) and sulpiride on dopamine (DA) biosynthesis in synaptosomes of the nucleus accumbens septi of the rat brain were studied. Carbidine caused a dose-dependent decrease of the animals' locomotor hyperactivity induced by apomorphine (1 mg/kg). Both carbidine and sulpiride administered in a dose of 5 mg/kg increased the activity of tyrosine hydroxylase in synaptosomes of the nucleus accumbens septi. In vitro carbidine decreased and sulpiride exerted no effect on the activity of tyrosine hydroxylase of the nucleus accumbens septi synaptosomes. Carbidine as well as sulpiride in vitro failed to modify the release of 3H-DA from superfused synaptosomes. At the same time, both in vivo and in vitro, the two neuroleptics reduced the inhibitory effect of DA on the 3H-DA release from synaptosomes of the nucleus accumbens septi and on the activity of tyrosine hydroxylase.

Animals↗
PubMedDate not supplied

[Effect of carbidine, sulpiride and haloperidol on levels of monoamines and their metabolites in the brain structures of rats].

Haloperidol (1 mg/kg) was shown to increase significantly the dopamine (DA) turnover in n. accumbens and striatum and to a lesser degree in frontal cortex and hypothalamus of the rat brain; to decrease the noradrenaline content in hypothalamus. Sulpiride (50 mg/kg) slightly increased DA turnover in striatum and hypothalamus and lowered the serotonin (5-HT) content in frontal cortex. Carbidine (25 mg/kg) was found to increase DA turnover in frontal cortex, striatum and hypothalamus to a greater degree than haloperidol; 5-HT turnover was increased in all the cerebral regions. The results obtained indicated that the atypical neuroleptic drug carbidine exerts the predominant effect on the frontal cortex, the serotoninergic component being clearly pronounced.

Animals↗
PubMedDate not supplied

[Effect of psychotropic substances and gamma-aminobutyric acid analogs and derivatives on the release of 3H-D-aspartic acid from perfused synaptosomes of the rat cerebral cortex].

It was shown in experiments in vitro that neuroleptics haloperidol and sulpiride, antidepressants desipramine and amitriptyline, nootropic agent piracetam, benzodiazepine tranquillizer phenazepam, psychostimulant phenamine and agonist of GABA A-receptors tetrahydroisoxazolopyridinol depending on the concentration in the micromolar range decrease K+-stimulated release of 3H-D-aspartic acid from rat brain cortex synaptosomes. Agonists of GABA B-receptors phenibut and baclofen as well as valproate and sodium oxybutyrate failed to exert a noticeable effect on the process under study.

Animals↗