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K S Rayevsky

Publications and source records attributed to K S Rayevsky.

7 recordsLinked to original sources
PubMed1992

Ethanol and delta-sleep-inducing peptide: effects on brain monoamines.

The brain content of dopamine (DA) and its metabolites [dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] were the same in rats with different immobilization times in forced swimming test, while the serotonin (5-HT) concentration was higher in high active (HA, immobilization < 2 min) than low active (LA, immobilization > 5 min) animals. Ethanol (2 g/kg, PO) tended to increase the DA level in the striatum and nucleus accumbens in LA rats and decrease the 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) concentration in HA rats. delta-Sleep-inducing peptide (DSIP) injection reduced the level of 5-HT in the medial prefrontal cortex (MFC) in both groups, did not affect the concentration of DA or DOPAC, but increased HVA in the striatum of HA rats. DSIP injected before ethanol administration augmented the ethanol effects on 5-HT in the MFC and attenuated the action of ethanol on 5-HIAA in the nucleus accumbens. A relationship between the different levels of voluntary alcohol consumption and sensitivity to stress among LA and HA rats and the differences in DA and 5-HT concentrations is suggested. The use of LA and HA rats in developing models for testing of stress-shielding compounds is also described.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Stereoisomers of the atypical neuroleptic carbidine modulate striatal dopamine release in awake rats.

Intracerebral microdialysis was used to monitor extracellular levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid and homovanillic acid in awake rats, after intraperitoneal administration of the cis- and trans-isomers (25 mg/kg and 1 mg/kg, respectively) of carbidine, the atypical neuroleptic drug, in comparison with sulpiride (50 mg/kg) and haloperidol (1 mg/kg). Trans-carbidine was found to be more potent than the cis-isomer in increasing the release of DA. In contrast to sulpiride and haloperidol, both isomers at the doses used, produced only a moderate elevation in the levels of the metabolites of DA. Transcarbidine seemed to be more potent as a neuroleptic drug, in comparison with the cis-isomer.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Cognitive deficiency induced by the acute stress in rats: a possible role of brain catecholaminergic systems.

The evaluation of the male albino rats cognitive capacity was performed by placing the animals in glass cylinder plundged into water (22 degrees C.) In order to escape from that stress situation the rat should dive under the cylinder's edge, solving by this way the extrapolatory escape task (EET). Two groups of rats (A and B) have been selected and characterized within the total laboratory population. The A rats have shown a smaller number of attempts to achieve successful escape and a shorter latency of that reaction in comparison with the B animals. The latter displayed a higher behavioral activity in "open field" test. The combination of 100 mg/kg L-DOPA with 25 mg/kg of benzerazide (DOPA-BENZ) was shown to impair dramatically the cognitive capacity of the two groups of animals. DOPA-BENZ treated rats failed to demonstrate any correct solution of EET. The rats of the two groups were distinguished clearly in terms of dopamine contents and turnover rate measured in three brain areas by the HPLC technique. Among psychotropic drugs studied only haloperidol and fluphenazine were found to restore partially the animals capacity to cope with the EET after DOPA-BENZ administration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Presynaptic dopamine and serotonin receptors modulating tyrosine hydroxylase activity in synaptosomes of the nucleus accumbens of rats.

Tyrosine hydroxylase (TH) activity was determined by measuring the formation of [3H]DOPA from [3,5-3H]tyrosine in the crude synaptosomal fraction of the nucleus accumbens under conditions preventing dopamine reuptake in 30 mM K+-containing medium. TH seems to be allosterically activated under depolarizing conditions: a 4.4 fold decrease of the Km value for tyrosine of the synaptosomal TH was observed. Synaptosomal TH activity was inhibited concentration dependently by dopamine and apomorphine resulting in IC50 values of 0.4 and 0.25 microM, respectively. The maximal inhibitory effects of dopamine as well as apomorphine were about 50% of the controls. The dopamine-induced inhibition was completely antagonized by neuroleptics. The rank order of antagonistic potencies was haloperidol greater than clozapine greater than sulpiride (with increasing EC50); methiothepine was ineffective. Moreover, synaptosomal TH activity was inhibited by serotonin in a concentration-dependent manner (IC50 = 0.8 microM). This inhibition was completely antagonized by methiothepine while, on the other hand, haloperidol was ineffective. The experimental system demonstrated here appears to be suitable for estimating the presynaptic dopamine and serotonin antagonistic potencies of drugs.

Animals↗
PubMed1978

Brain tyrosine hydroxylase: kinetic properties and regulation of the activity.

Electrical stimulation of rat hypothalamic synaptosome suspensions produced activation of tyrosine hydroxylase due to increase of the affinity for tyrosine and 6,7-dimethyl-5,6,7,8-tetrahydropterine cofactor, decrease of the affinity for dopamine and enhancement of substrate inhibition. Cocaine (10(-7) - 10(-5) M) in vitro caused enzyme activation; when administered to animals systemically (0.5 mg/kg) the drug produced inhibition of hypothalamic tyrosine hydroxylase probably through a receptor-mediated feedback mechanism.

Animals↗
PubMed1978

The effect of neuroleptics on brain tyrosine hydroxylase.

The effect of a number of neuroleptics and tricyclic antidepressants on the activity of rat hypothalamic tyrosine hydroxylase was studied utilizing a direct spectrophotometric method. All the neuroleptics (but not the antidepressants) were able to reverse the substrate inhibition of the enzyme occurring when the tyrosine concentration in the medium was increased. Haloperidol, haloanisone and fluphenazine were found to activate the enzyme at optimal tyrosine concentrations in contrast to other neuroleptics which reduced the enzyme activity. The systemic administration of fluphenazine and clozapine was followed by an increase in the activity of striatal and hypothalamic tyrosine hydroxylase. The same drugs failed to produce this effect when administered chronically for 8 days.

Amitriptyline↗