[The action of befol and its derivatives on monoamine oxidase of different origins]. / Deistvie befola i ego proizvodnykh na monoaminoksidazu razlichnogo proiskhozhdeniia.

The effect on deamination of serotonine, dopamine, tiramine and 2-phenylamine of benzamide derivatives befol, moclobemide and LIS-641 was studied. Befol and moclobemide are inhibitors of serotonine deaminating activity of MAO. The different sensitivity of this activity to the effect of the benzamide derivatives in beef or rat brain and human placenta was noted. The inhibition was more distinct in tissue homogenate than in corresponding mitochondrial fractions.

[Nootropic activity of nicotinamide and its structural analogs]. / Nootropnaia aktivnost' nikotinamida i ego strukturnykh analogov.

It is known that endogenic nicotinamide has a tranquilizing and stress-protective activity. The present investigations show the nootropic effect of this drug and its analogs nicomorpholine and acethylnicotinate on acute models of hypoxia and amnesia. The present results revealed that the observed nootropic activity of nicotinamide and its analogs is more expressed than this of piracetam, pyritinol and meclofenoxate. Having in mind the similarity of pharmacological effects of piracetam and nicotinamide (antihypoxic, antiamnestic and anxiolytic) we try if these drugs have electronic-structure similarities. The analysis revealed some similarity of these drugs' molecules in relation to the composition and distribution of polar centres pi- and p-electronic areas) distance between them, topography of separate molecule parts.

[Lipid peroxidation in the caudate nuclei in experimental parkinsonian syndrome]. / Perekisnoe okislenie lipidov v kvostatykh iadrakh pri éksperimental'nom parkinsonicheskom sindrome.

Lipid peroxidation was investigated in adult (8-10 months of age) rat striatum with Parkinsonian syndrome induced by MPTP and its metabolite MPP+. MPTP 20 mg/kg i.p. 4 doses) produced a slight enhancement of lipid peroxidation and significant increase when MPP+ (0.04 mg/kg) was injected into the substantia nigra.

[Reception and extrareceptor binding of cytostatic serotonin antagonists by early embryos of the sea urchin Arbacia lixula]. / Retseptsiia i vneretseptornoe sviazyvanie tsitostaticheskikh antagonistov serotonina rannimi zarodyshami morskogo ezha Arbacia lixula.

Unfertilized eggs and early embryos of the sea urchin Arbacia lixula incubated for 60 min in a medium containing the antagonists of prenervous serotonin, i.e. inmecarb (21 microM) or imipramine (40 microM), bind up to 5 microM of these drugs per 1 ml of cells. At high cell concentrations (more than 10,000 eggs or embryos per 1 ml), this binding is not followed by inhibition of cleavage divisions or by increase in the sensitivity to cytostatic effects of these drugs, which is taken as an indication that this binding is a nonreceptive one. The decrease in concentration of eggs or embryos does not affect total binding of the drugs, although their antiserotonin effects become evident indicating the existence of the receptor sites of binding. In experiments with 3H-imipramine, two binding pools were found (Bmax being correspondingly equal to about 20 and 0.75 microM/ml of embryos; the values of Kd amount to 200 and 15 microM). One of them is a nonreceptive pool, whereas the other presumably coincides with receptor binding sites of prenervous serotonin antagonists.

[Experimental parkinsonian syndrome in rats induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine]. / Eksperimental'nyi parkinsonicheskii sindrom u krys, vyzvannyi 1-metil-4-fenil-1,2,3,6-tetragidropiridinom.

Systemic administration of high doses of MPTP caused transient bradykinesia, "freezing" episodes, head tremors, hunching of the back and peripheral autonomic effects. Neurological syndrome was clearly dose-dependent. It has been established that Parkinson's syndrome is caused by high-amplitude paroxysmal discharges in the nucleus caudatis. It is concluded that the nucleus caudatis plays the role of a pathological determinant structure in the development of Parkinson's syndrome induced by MPTP.

[Effect of benzamide derivatives on convulsions induced by the toxic action of oxygen in rats]. / Vliianie proizvodnykh benzamida na sudorogi, vyzvannye toksicheskim deistviem kisloroda u krys.

The reversible MAO-A inhibitor moclobemide (5 mg/kg) was shown to prevent seizures in rats during exposure to toxic oxygen (6 ata). Benzamide derivatives increased the latent period of oxygen seizures and decreased the lethality following hyperbaric oxygenation. The range of anti-MAO activity of moclobemide and clorgyline in the rat brain and heart after toxic oxygenation was studied. It was distinct from those in control animals. Clorgyline was found to be more active in inhibiting MAO during toxic oxygenation in the heart and moclobemide-in the brain. The possibility is shown to prevent oxygen seizures not only with irreversible MAO-A inhibitors (clorgyline), but also with reversible ones (moclobemide).

[Effect of benzamide derivatives on rat brain monoamine oxidase activity in vitro]. / Vliianie razlichnykh proizvodnykh benzamida na aktivnost' monaminoksidazy mozga krysy in vitro.

The ability of moclobamide and other benzamide derivatives to inhibit the activity of monoamine oxidase in the rat brain was studied. Distinct effects of these compounds on the deamination of serotonin and norepinephrine (MAO-A substrates); 2-phenylethylamine (selective MAO-B substrate); tyramine and dopamine (MAO-A and MAO-B substrates) are shown. It was demonstrated that among all the compounds studied moclobamide appeared to be the most active and selective inhibitor of MAO-A: at a concentration of 100 microM it caused a 100% inhibition of serotonin and norepinephrine deamination, which might be explained by the presence of C1 atom in the para-position of benzene ring in moclobamide molecule. Other benzamide derivatives were less active in inhibiting MAO-A and had but a negligible effect on dopamine- and 2-phenylethylamine deamination.

[Dynamics of the inflammatory process caused by carrageenin administration during experimental therapy]. / Dinamika protsessa vospaleniia, vyzvannogo vvedeniem karagenina, pri éksperimental'noi terapii.

Carrageenan is shown to cause acute inflammation in mucous membrane of hamster cheek pouch and rat hind foot. Rutin has no effect on the pathological process in the cheek pouch, and arrests the first phase of inflammation in the foot. Esculamine has a therapeutic effect on both phases of inflammatory reaction in the cheek pouch and foot.

[Effect of rutin and esculamine on models of aseptic inflammation]. / Vliianie rutina i éskulamina na nekotorye modeli aspeticheskogo vospaleniia.

It was shown in experiments on rats that intraabdominal administration of silver nitrate solution induces peritonitis and the subplantar administration of histamine, serotonin and prostaglandin E2 leads to an acute paw edema. Preliminary subcutaneous administration of esculamine or rutin inhibited the development of the inflammation. Esculamine proved more active here.

[Behavioral and radioreceptor analysis of viloxazine stereoisomers]. / Povedencheskii i radioprotektornyi analiz stereoizomerov viloksazina.

The differences in the pharmacological effects of R(+)- and S(-)-isomers of the atypical antidepressant viloxazin were discovered in two behavioral models. The S(-)-isomer appeared 5 times as active as the R(+)-isomer under acute administration. In chronic administration, (15 days), the R(+)-isomer appeared ineffective. Comparison of the affinity of the racemate, R(+) and S(-)-isomers for alpha 1-, alpha 2- and beta-adrenoreceptors, as well as for serotonin, C1, benzodiazepine, imipramine and dopamine receptors did not demonstrate any stereospecificity of viloxazin isomers. It is assumed that some other receptors (histamine, acetylcholine) present the targets for the pharmacological action of viloxazin or the latter one has, like zimelidin , specific binding sites of its own.