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Biomedical subjects

A N Kharlamov

Publications and source records attributed to A N Kharlamov.

10 recordsLinked to original sources
PubMed1987

[Effect of sidnocarb on learning and memory].

It has been established that in well-trained rats sydnocarb (mesocarb) does not exert a considerable effect on the generation of conditioned reflex of passive avoidance (CRPA). On the contrary, in poorly-trained animals sydnocarb significantly improves CRPA indexes at all three stages of its generation. Sydnocarb proved most effective, when injected before training (on day I). The absence of sydnocarb-induced pain threshold decrease in response to electrical pain stimulation suggests a direct drug effect on memory processes.

Animals↗
PubMed1985

[Anxiolytic action of sodium valproate (possible role of gamma-aminobutyric acid in affective disorders)].

An experimental and clinico-pharmacological study of sodium valproate, a GABA-ergic drug, was conducted to elucidate the role of gamma-aminobutyric acid in the mechanisms responsible for affective disturbances, in particular for anxiety. A tranquilizing effect of the drug, comparable with the action of diazepam, was established in a conflict situation model in experimental animals. Using clinico-psychological methods the authors showed a distinct tranquilizing action of valproate in patients suffering from neurotic and neurosis-like disorders with manifestations of anxiety in the structure of the psychopathological syndrome. It was established that this action was accompanied by no manifestations of myorelexation, ataxia or somnolence characteristic of tranquilizers of the benzodiazepine series. The presence of tranquilizing properties in the GABA-ergic drug sodium valproate confirms the suggestion that a certain relationship exists between the GABA system and anxiety.

Adult↗
PubMed1983

GABA-ergic drugs: effects on conditioning, memory and learning.

In order to study the role of GABA in behaviour, various GABA-mimetic and GABA-blocking drugs were tested for their effects on a conditioned avoidance response (CAR). Sodium valproate slowed the acquisition of CAR and failed to affect the latency of a well-learned CAR, but interestingly, showed a marked anti-conflict effect similar to that of benzodiazepine-derivatives. The similarity of effects of drugs such as benzodiazepines and sodium valproate, which are postulated to potentiate GABA-ergic transmission, suggests that GABA plays a role in conditioning, memory and learning.

Aminooxyacetic Acid↗
PubMed1981

[Role of the GABA-ergic link in the development of the tranquilizing effect in cats].

The development of the tranquilizing effect of n-dipropylacetate (n-DPA) selectively increasing the GABA level in the nerve terminals was studied in experiments on cats in comparison with diazepam effect. The changes in the spectrum of emotional-behavioral reactivity were estimated. In doses of 50 and 200 mg/kg n-DPA caused a marked antiphobic effect which was not accompanied by the activating component characteristic of diazepam. The n-DPA-induced increase in the GABA level in the nerve terminals is suggested to be important for the development of the anxiolytic effect of tranquilizers. The total increase in the GABA level in the nerve terminals is suggested to be important for the development of the anxiolytic effect of tranquilizers. The total increase in the GABA content in the brain correlates to a greater extent with the sedative effect of drugs.

Animals↗
PubMed1980

[Tranquilizing effect of n-dipropylacetate and other GABA-ergic substances in conflict situations].

Effect of n-dipropyl acetate (n-DPA), amino oxyacetic acid (AOAA), pantogam and piracetam on rat behaviour was studied under conflict situation. n-DPA, AOAA and piracetam increased significantly the main index of the tranquilizing action, that is the number of water intakes from the drinking bowl, supported by electric stimulation. This effect was most pronounced in n-DPA. Bicuculline and corasol almost completely eliminated the tranquilizing effect of n-DPA, while this effect was abolished by caffeine only by 50%.

Acetates↗
PubMedDate not supplied

[Effect of sodium valproate on the mediator amino acid content in the rat brain].

The effect of sodium valproate (200 mg/kg, intraperitoneally) on the content of transmitter amino acids in the large hemispheres, hippocamp and thalamus was studied in experiments on rats. Thirty minutes after the injection no appreciable shifts in the content of GABA or glutamate were recorded in homogenates of these structures. However, this does not exclude the effect of sodium valproate in the dose mentioned on the GABA system at the expense of changes in the compartmentation of GABA. The concentration of aspartate was found to be significantly decreased in all the brain structures under study. It is suggested that these changes in the aspartate system might be related to the realization of the tranquilizing effect of valproate since they coincided in time with the behavioral effects of the drug.

Amino Acids↗
PubMedDate not supplied

[Lithium valproate: its neuropharmacological spectrum and effect on transmitter amino acid content of the brain of rats].

The authors studied lithium valproate synthesized at the Institute of Pharmacology, Academy of Medical Sciences of the USSR, and compared it with sodium valproate (depakin, France). It was discovered that like sodium valproate, lithium valproate has a marked anticonvulsant activity, being also effective in experimental seizures induced by bicucullin, exerts a moderate sedative action (potentiation of sodium thiopental and hexenal anesthesia), and a distinct tranquilizing effect in experimental outward inhibition of the conditioned active avoidance response. At the same time the presence in the molecule of lithium ions led to a change in the neurochemical profile of valproate, manifested by an increase in the rat brain content of GABA and glutamate.

Amino Acids↗
PubMedDate not supplied

[GABA-ergic component in the mechanism of action of the psychostimulant sidnocarb].

The psychostimulant sydnocarb administered in single doses of 15 and 25 mg/kg provokes a dose-dependent decrease in the brain GABA content without affecting the concentration of glutamate and aspartate. This effect remains unchanged but does not get potentiated after combined use of sydnocarb and thiosemicarbazide. During chronic 2-week administration of sydnocarb, a significant reduction in the GABA and aspartate content in the brain is detected. The GABA-positive substance valproate does not prevent the stimulant effect of sydnocarb on the motor and orienting activity of animals under "open field conditions". However, the research behavior remains in this case depressed. Sydnocarb reduces, whereas amphetamine prolongs the latent period of GABA-deficient seizures induced by thiosemicarbazide. The biochemical and behavioral data suggest that the GABA-ergic component is involved into the mechanism of the psychostimulant action of sydnocarb.

Amphetamine↗
PubMedDate not supplied

[Effect of GABA-ergic substances on the conditioned avoidance reaction in rats].

The effect of GABA-ergic substances on the production and latent period of the conditioned reflex of avoidance in rats has been studied. The inhibitor of GABA-transaminase n-dipropylacetate (depakin) deteriorates the reflex production. Fenibut and amino oxyacetic acid significantly prolong the latent period of the produced conditioned reflex of avoidance. The effect of amino oxyacetic acid on the conditioned reflex is abolished by bicuculline and is likely to be related to the increased brain GABA content.

Animals↗