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Biomedical subjects

R U Ostrovskaia

Publications and source records attributed to R U Ostrovskaia.

At least 55 records · Page 3Linked to original sources
PubMed1980

[Participation of GABA-ergic structures in producing the effects of haloperidol].

A study was made of the effect of haloperidol on convulsions induced in mice by bicuculline and thiosemicarbazide and on the recovery cycles of the primary response in the rat sensorimotor cortex. In doses of 0.3--0.5 mg/kg producing a tranquilizing effect, haloperidol exerts a protective action in convulsions induced by bicuculline blocking of the GABA receptors and enhances the depression of the testing response during recovery cycle of the rat sensorimotor cortex primary response. It means that over this dosage range haloperidol potentiates GABA-induced effects. An increase in the neuroleptic dose up to 1--2 mg/kg entails disappearance of the efficacy shown by both the tests. The authors' own and reported data suggest an important role played by the postsynaptic GABA-positive effect in realization of the tranquilizing action of haloperidol and other neurotropic agents.

Animals↗
PubMed1980

[Effect of sodium hydroxybutyrate on the ammonia level in the rat muscles under physical exercise].

The experiments on rats exposed to compulsory swimming have shown the normalizing effect of sodium hydroxybutyrate with respect to one of the biochemical indices of physical overwork: the ammonia level in cross-striated muscles. In control rats who had not received the drug, the swimming induced a significant (more than twofold) increase in the muscle tissue ammonia level, whereas animals preventively treated with sodium hydroxybutyrate (single administration or two-week course) demonstrated no ammonia accumulation. It is suggested that sodium hydroxybutyrate preventing the toxic effect of one of the end products of nitrogen metabolism may reduce afteraction of muscular overwork.

Ammonia↗
PubMed1979

[Effect of GABA-ergic substances on the analgesic effect of morphine in rats].

The effect of GABA-ergic compounds on morphine-induced analgesia was studied to reveal probable interaction of GABA and opiates. As an index for morphine effect the reaction of vocalization in response to electrical stimulation of the rat tail was used. It was shown that thiosemicarbazide, the inhibitor of glutamate decarboxylase and bicuculline, GABA-ergic receptor blocking agent, which were proposed to be joined in a group of GABA-negative compounds, reduce and shorten the effect of morphine. Depakine, the inhibitor of alpha-ketoglutarate-GABA-transaminase, as well as GABA itself administered in high doses (GABA-positive actions) make morphine analgesia more pronounced and longer. Probable causes of the described interrelationship between GABA and opiates are discussed.

Analgesia↗
PubMed1978

[Participation of cholinergic mechanisms in realizing the effects of bicuculline].

Screening and electrophysiological methods were applied to the verification of the hypothesis on a possibility of participation of cholinergic structures in the realization of bicucullin effects. M- and N-cholinolytics (benactizine, atropine, aprophen, and pediphen) failed to arrest the convulsions induced in mice by bicucullin adminstration. At the same time substances inducing accumulation of gamma-aminobutyric acid (GABA) in the brain, i.e. aminooxycetic acid and depakin produced a manifest protective action in convulsions caused by bicucullin administration. In electrophysiological experiments there was also revealed an incapacity of M-cholinolytic benaltizine to arrest the bicucullin effects. Bicucullin proved to diminish depression of the test response in the restoration cycle of the primary response of the rat sensory motor cortex at the intervals of 40--125ms between the stimuli, whereas benactizine decreased the late facilitation of the test response at the intervals of 150--300ms between the stimuli. There was also noted no interaction between benactizine and bicucullin by this test. On the basis of these data a conclusion was drawn that bicucullin effects were caused by the block of postsynaptic GABA receptors, and were not connected with the cholinergic structures activity.

Animals↗
PubMed1978

[Effect of cesium, lithium and rubidium on several effects of morphine].

The effect of chlorous salts of cesium, lithium, and rubidium on the analgetic action of morphine (according to the vocalization test) and also on the pattern of the dependence on it (according to the so-called "two-bottle test") was studied. As shown, the salts under investigation decreased both the algesic reaction threshold and the duration of morphine-induced analgesia; cesium chloride proved most active in this respect. All the compounds studied decrease the morphine preference coefficient. The greatest effect was found in cesium chloride which decreased the morphine preference coefficient 40-fold as compared to the control.

Animals↗
PubMed1977

[Inhibitory processes in the cerebral cortex and the anticonvulsive action of benzodiazepine derivatives].

A comparative study of the effect of some benzodiazepine deprivatives (chlonazepam, lorazepam, diazepam, and medazepam) on the recovery cycles of the interzonal response was carried out on unanesthetized curare-immobilized cats. These drugs proved to selectively inhibit the testing potential within the range of 20 to 100 msec. between the conditioning and the testing stimuli. This indicates that potentiation of GABA-ergic inhibition in the cerebral cortex. The threshold doses of the drugs inducing the depression of the test response and of ED50, preventing the development of convulsions, caused by GABA deficiency or by GABA-ergic receptor block, were compared; a correlation between the mentioned effects was demonstrated. The significance of GABA-positive effect of benzodiazepines in the mechanism of their anticonvulsive activity is suggested.

Animals↗
PubMed1977

[Effect of diazepam on the impulse activity of neurons in the sensomotor and visual areas of the rat cerebral cortex].

Acute experiments on nonanesthetized curare-treated rats with the recording of the neuronal activity of the cortex were conducted; a determination was made of the threshold doses in which diazepam influenced the spontaneous and induced activity of the neurons of the sensory-motor and optic cortex. Diazepam proved to depress the spontaneous and induced activity of the neurons of the sensory-motor and optic cortex. Diazepam proved to depress the spontaneous and induced activity of the neurons of the sensory-motor cortex in considerably lesser doses than the neuronal activity of the optic cortex. It is supposed that the neurons of the anterior portions of the cortex were more sensitive to diazepam than the neurons of the limbic structures and the reticular formation.

Animals↗
PubMed1977

[Antagonistic effect of bicuculline and thiosemicarbazide on the tranquilizing effects of diazepam].

It has been shown that bicuculline--GABA-ergic receptors specific blocking agent in doses of 0.5 and 1.0 mg/kg (subcutaneously), and thiosemicarbazide (inhibiting the brain GABA synthesis) in dose of 5.0 and 8.0 mg/kg (subcutaneously) were capable of antagonizing diazepam effects and of reducing its tranquilizing activity in an experimental test of conflict behavior in rats. Bicuculline exhibited a more pronounced antagonism to diazepam than thiosemicarbazide. The data obtained testified to a possible involvement of the GABA-ergic mechanisms in the realization of the anxiolytic effect of benzodiazepines.

Animals↗
PubMed1976

[Increase in the sensitivity of rabbit sensomotor cortex neurons to gamma-aminobutyric acid under the influence of diazepam (microiontophoretic study)].

A study was made of the action of diazepam on the effects of the gamma-aminobutyric acid (GABA) applied electrophoretically to the neurons of the sensory-motor rabbit cortex. It was shown that diazepam intensified the depressive action of GABA on the spontaneous neuronal activity and the prolonging action of GABA on the duration of the inhibitory phase in the neuron responses to the afferent and direct stimulation of the cortex. Diazepam failed to alter the neuron response to glycine, glutamate and acetylcholine applied microelectrophoretically. It is supposed that diazepam increased the sensitivity of the receptors of the post-synaptic membrane of the neuron to GABA.

Aminobutyrates↗
PubMed1976

[GABA-ergic mechanism of action of diazepam on cerebral cortex neurons].

The effect of diazepam, depakin, thiosemicarbazide (TSC) and bicucullin on the spontaneous and incuced (by stimulation of the sciatic nerve) activity of the cells of the sensory-motor cortex was studied on the unanesthetized immobilized (curarized) albino rats. Diazepam proved to intensify the inhibitory phenomena, i.e. decreased the frequency of spontaneous discharges and prolonged the postactivation depression of the neuron impulsation (the inhibitory pause. Depakin increasing the GABA content in the brain acted similarly. The GABA-ergic receptors blocker, bicucullin and TSC, decreasing its content, on the contrary, weakened the inhibitory phenomena. There was also revealed a reversible antagonism between diazepam and bicucullin in their effect on the neuronal activity. The data obtained confirmed the supposition put forward formerly on the capacity of diazepam to intensify the effect of GABA on the neurons of the cerebral cortex.

Aminobutyrates↗
PubMed1976

[Effect of succinic semialdehyde on nitrogen metabolism of animal brain tissue during hypoxia].

In examining the content of free ammonia, glutamine and some free amino acid s in the brain tissue of mice under normal conditions, in hypoxia and under the effect of succinic acidsemialdehyde, in hypoxia there was revealed a marked increase in comparison with the normal conditions) of the content of free ammonia, and alpha-alanine, a reduction of glutamine; there was also a slight elevation in the content of gamma aminobutyric acid and no changes in glutamic and asparagic acid content. In case of pretreatment with succinic acid semialdehyde the content of free ammonia, glutamine and alpha-alanine in hypoxia approached the normal value. One of the possible mechanisms of the antihypoxic effect of succinic acid semialdehyde was transformation of this compound as a results of which there occurred synthesis of glutamic acid and glutamine leading to detoxication of free ammonia accumulating in the brain tissue in hypoxia.

Alanine↗
PubMed1975

[Effect of carbidine on conditioned defense reflexes].

Chronic experiments were conducted on rats and rabbits; a study was made of the effect of carbidine on the conditioned defence reflexes in stimulation of the mesencephalic part of the reticular formation. Carbidine prevented the depression of the conditioned defence reflexes caused by stimulation of the mesencephalic portion of the reticular formation. This pointed to its depressive influence on the mentioned structures, and was confirmed by experiments on rabbits in recording changes in biocurrents under conditions of stimulation of the mesencephalic reticular formation.

Animals↗
PubMed1975

[The mechanism of the anticonvulsive action of diazepam].

Diazepam was shown to be highly efficient in preventing the convulsive siezures induced by thiosemicarbazide and connected with GABA insufficiency. In recording the recovery cycles of the intracortical response of the cat motor cortex it was found that diazepam induced a decrease of the testing respone. These data indicate the enhancement of the inhibitory processes. Using this test an antagonistic relationship was observed between diazepam on the one hand, and biculline and thiosemicarbazide--on the other Diazepam was capable of increasing GABA content in the brain by suppressing GABA-transaminase activity in the mitochondrial fraction of the brain tissue.

Aminobutyrates↗
PubMed1975

[Antagonistic effect of sodium hydroxybutyrate on several effects of aminoxyacetic acid].

A well-known protective effect of aminooxyacetic acid against thiosemicarbazide convulsions was confirmed; it was shown that a similar, although somewhat weaker activity, was exerted by sodium hydroxybutyrate. Surprisingly, the effect of aminooxyacetic acid was diminished by sodium hydroxybutyrate. Sodium hydroxybutyrate in combination with aminooxyacetic acid decreased the protective activity of the latter against thiosemicarbazide convulsions and diminished the extent of GABA accumulation characteristic of aminooxyacetic acid action. This effect is attributed to the competition between the aminooxyacetic acid, sodium hydroxybutyrate and GABA for alpha-ketoglutarate-GABA-transaminase and possible for the GABA-ergic receptor.

Acetates↗