Effects of N-acetyl-aspartic acid (NAA) on the behaviour models "open field", passive avoidance test and content of monoamines and their metabolites in the brain areas on the 9-th day after frontal decortication were studied. NAA (50 mg/kg), i.p., daily, 9 days) exerted antiamnestic effect in decorticated rats, evaluated in passive avoidance test. Corresponding changes in concentration of serotonin and 5-hydroxyindolacetic acid in the brain of decorticated rats were also seen.

Amnesia↗

PubMed1993

[The evaluation of the effects of piracetam and N-acetylaspartic acid on memory and the content of mediator amino acids in the brain in a model neurotic state in rats].

The model neurotic state in rats was formed within 1 month by the method of "conflict of afferent excitations". Piracetam and N-acetyl aspartic acid in doses of 250 and 50 mg/kg, respectively, administered intraperitoneally daily for the last 7 days of the experiment prevented the amnesia of the passive avoidance habit, which is typical of the developed abnormality in 60 and 40% of the rats, respectively (p < 0.05). The neurotic state was characterized by a significant increase of contents of inhibitory amino acids GABA and glycine in the brain cortex, GABA and glutamate in the hippocampus. Piracetam caused inversely directed changes of these parameters in the neuroticized animals.

Amino Acids↗

PubMed1992

[Neurochemical strategy in the study of the mechanism of action of currently used antipsychotic drugs].

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Animals↗

PubMed1992

[Different effects of typical and atypical neuroleptics on K+-stimulated dopamine release from isolated rat striatum].

Effects of haloperidol (10(-7)-alpha 10(-5) M), trifluoperazine, metoclopramide, tiapride, sulpiride, thioridazine, clozapine remoxipride, raclopride, cis- and trans-isomers of carbidine, SCH 23390 (all at the 10(-6) M) on the K(+)-stimulated (28 mM) dopamine (DA) release from isolated rat striatum were studied. Haloperidol at the concentration of 10(-7) and 10(-6) M failed to affect, while at 10(-5) M the drug decreased the stimulated striatal DA release. Trifluoperazine, metoclopramide and tiapride were shown not to modify this process. Sulpiride, thioridazine, clozapine, remoxipride, raclopride, isomers of carbidine were found to increase significantly the stimulated striatal DA release. SCH 23390 failed to affect K(+)-stimulated release of DA in the striatum and also did not change K(+)-stimulated release enhancement produced by raclopride. It is suggested that the mechanism underlying observed effects of the drugs may contribute to pharmacological profile of atypical neuroleptics.

Animals↗

PubMed1992

[Selective analyzers of dopamine D2 receptors modulate serotonin metabolism in the striatum and nucleus accumbens of the rat brain during blockade of dopaminergic impulse flow].

Effects of D2 dopamine receptor selective agonists: quinpirole (0.1, 0.3 and 1 mg/kg, i. p.), pergolide (0.3 mg/kg, i. p.), lisuride (0.1 mg/kg, i. p.) and antagonist raclopride (1.2 mg/kg, i. p.) on the metabolism and synthesis of DA and serotonin in the rat brain striatum and nucleus accumbens after GBL treatment were studied. GBL as well as dopamine D2 receptor selective drugs were shown not only to change neurochemical parameters of dopaminergic brain systems, but also to modulate serotonin metabolism without affecting its biosynthesis.

4-Butyrolactone↗

PubMed1992

[A comparative study of the neurochemical profiles of remoxipride, raclopride and metoclopramide activity].

Effects of intraperitoneal administration of remoxipride (2.4 mg/kg), raclopride (1.2 mg/kg) and metoclopramide (5 mg/kg) on the concentration of monoamines and metabolites in various brain regions, on the DA and serotonin biosynthesis in the striatum and nucleus accumbens, on the K(+)-stimulated DA release from the isolated striatum, on the extracellular levels of DA and metabolites in the striatum of freely moving rats were studied. Remoxipride and raclopride increase DA turnover, biosynthesis and DA release, studied both in vitro and in vivo. Metoclopramide was shown to be more effective in increasing DA turnover and biosynthesis, while exerted less activity in regard to increasing DA release in vivo and failed to affect release in vitro. Possible neurochemical mechanisms underlying pharmacological effects of these drugs are discussed.

Animals↗

PubMed1992

[Psychotropic properties of brain proline endopeptidase inhibitors].

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Animals↗

PubMed1991

[An experimental study of the antidepressive properties of captopril].

Captopril, as well as amitriptyline, was shown to enhance apomorphine-induced stereotype in mice. At doses, which failed to modify the effect of apomorphine, both substances reversed the inhibitory action of sulpiride and haloperidol on stereotypical behaviour. Treatment with captopril (25 mg/kg) did not modify the open-field behaviour, but significantly reduced the immobility in the forced swim test (20 mg/kg) Dopaminergic link was suggested to be involved in the CNS effect of captopril.

Amitriptyline↗

PubMed1990

[Effects of antidepressive agents on glutamatergic autoregulatory presynaptic mechanism in the rat cerebral cortex].

Amitriptyline, imipramine, desipramine, viloxazine, moclobemide and its derivative, novel antidepressant befol (10(-6)-5 x 10(-4) M) decreased by 12-20% K(+)-stimulated 3H-D-asp release from perfused synaptosomes of rat brain cortex. Glutamic acid diethyl ester (GDEE) (10(-4) M) antagonized the effect of amitriptyline, imipramine, desipramine and befol and reversed the effect of moclobemide and viloxazine. Among neuroleptics studied, only carbidine, which possesses antidepressant activity together with antipsychotic one in clinics, decreased 3H-D-asp release by GDEE-sensitive mechanism. Effect of haloperidol and chlorpromazine was not affected by GDEE. It is concluded that autoregulatory mechanism on the terminals of glutamatergic neurons may be involved in the antidepressant action.

Animals↗

PubMed1990

[Effect of ethanol on the levels of dopamine and its metabolites in the brain of rats with different degree of sensitivity to stress].

It was shown, that content of dopamine and its metabolites (DOPAC and HVA) are the same in two groups of rats with different time of immobilization in forced swimming test. One group of low active (LA) animals experienced the immobilization more than 300s, other high active (HA) rats for less than 120 s. Ethanol (2 g/kg per oris) increased the level of DA in the striatum and medial prefrontal cortex only in LA rats and besides, the concentration of dopamine after ethanol administration was higher in the n. accumbens of LA rats, than in that of HA rats. The authors suggest that differences in dopamine content between LA and HA rats are connected with different levels of voluntary alcohol consumption. The opportunity to use both groups of HA and LA rats for developing models of pathogenic heterogeneity of alcoholism is discussed.

3,4-Dihydroxyphenylacetic Acid↗

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↗