PubMed Health⌕ Search

Biomedical subjects

M A Gerebtzoff

Publications and source records attributed to M A Gerebtzoff.

At least 19 recordsLinked to original sources
PubMed1982

[Study of histoenzymologic signs of selective neuronal hyperactivity].

Injection of kainic acid into the cerebellum leads to a neuroexcitatory and neurotoxic effect on neurons connected with cerebellar granule cells. Observation of the activities of dehydrogenases taking part in glucose metabolism and glutamate dehydrogenase shows that Purkinje cells undergo a rapid destruction. Lesions of small stellate cells come later. But the basket cells present a long period of hyperactivity revealed by an increase of dehydrogenase activity.

Animals↗
PubMed1981

[Histochemical study of central nervous system lesions in experimental epilepsy caused by kainic acid].

In former investigations on human focal epilepsy and on experimental epilepsy by cobalt implantation, the authors have demonstrated the signaletic importance of "activated astrocytes": cortical astrocytes endowed with a modified metabolism and an accelerated turnover. The present study concerns the results of the intra-amygdaloid injections of kainic acid, a strong excitatory and neurotoxic amino acid. Injections in semi-chronic conditions in the rat lead to electrical and motor seizures and to the production of activated astrocytes not only in regions that might trigger off epileptic seizures (cerebral cortex, amygdala, possibly hippocampus), but also in the neostriatum. Stimulation of this last region results in a Huntington chorea-like syndrome. Thus, the importance of activated astrocytes must be extended to include other conditions of intense hyperactivity of neurons than epilepsy.

Animals↗
PubMed1979

[Selective fixation of methylselenobenzoic acid by the pineal gland].

Investigation of the localization in the central nervous system of the rat of an epileptogenic agent, methylseleno-2-benzoic acid, did not lead to its selective distribution in the cerebral cortex or in the brainstem in relation with its biological activity. But a systematic study of the distribution of this compound labelled with 75Se at a high specific activity has revealed a rate of fixation by the pineal gland 4 to 5 times higher than that of other tissues of the central nervous system. After a survival time of 4 hours, the radioactivity of the pineal gland exceeds that of the blood. A parallel study of the distribution of the 75SeO3- ion on the one hand of the 35S homolog of the 75Se compound on the other hand has demonstrated that the fixation by the pineal gland is bound to the molecular structure of the selenium compound.

Animals↗
PubMed1979

[The activity of cytochrome oxidase in the normal cerebral cortex and after destructive and irritating lesions. Histochemical research].

Production of an epileptogenic focus by cobalt-gelatin implantation in the cerebral cortex of the rat determines a local increase of cytochrome oxidase activity in neurones and probably a decrease of its activity in neuroglia. This variation of oxidative metabolism is not characteristic of the "epileptic neuron" since it takes also place after non irritative lesions, though remaining less conspicuous and less extensive.

Animals↗
PubMed1978

Histochemical study of cobalt-induced focal epilepsy.

A previous study showed a strong relationship between human focal epilepsy and the presence in the cortex of "activated" astrocytes characterized by an intense activity of dehydrogenases (DH) involved in glucose metabolism and of glutamate DH. Using the semi-chronic model of cobalt-induced experimental focal epilepsy in the rat, we investigated a possible correlation between astrocyte modifications and the chronological development of the epileptic manifestations on the ECoG. After a few days the cobalt-implanted rats present spikes, then sharp waves followed by an electrical crisis and ultimately motor seizures. Activated astrocytes were found in each phase of this evolution. Their number increases with the intensity of the manifestations. There is a close relationship between activated astrocytes and focal epileptic phenomena. At this stage of our study it is clear that the presence of activated astrocytes is not a consequence of seizures. However, it is impossible to say whether the activation is secondary to the hyperactivity of the neurons or directly responsible for the constitution of the epileptic focus. In any case, activated astrocytes provide a new means of localizing an epileptogenic focus.

Animals↗
PubMed1978

[Phosphorylase and glucosyltransferases at the level of reactive astrocytes. A histochemical study].

Implantation of cobalt powder in the cerebral cortex of rat determines an epileptogenic focus where two types of reactive astrocytes are observed. The first type is mostly represented in the subcortical white matter but it does exist in the cortex around the implant. Phosphorylase and branching enzyme are both very active in these cells which are filled with glycogen. The second type is limited to the cortex and phosphorylase activity leads to an unbranched polysaccharid. These cells correspond to the "activated astrocytes" described by the authors in a previous paper and observed round irritative lesions which, in the cerebral cortex, produce epileptogenic foci.

1,4-alpha-Glucan Branching Enzyme↗
PubMed1977

Action of phenytoin, ethosuximide and of the carbidopa-L-dopa association in semi-chronic cobalt-induced epilepsy in the rat.

A semi-chronic model of cobalt-induced experimental epilepsy in the rat was used to investigate the action of two classic anticonvulsant drugs, phenytoin and ethosuximide. Single injections of ethosuximide lead to an inhibition of the epileptic discharges. We failed to demonstrate an inhibitory effect of phenytoin after preventive administration. The carbidopa-L-dopa association was investigated owing to the inhibitory effects of dopamine and its presence in the cortex. We showed that a dose of 100 mg/kg of L-dopa combined with 25 mg/kg of carbidopa is necessary and sufficient to produce an almost complete inhibition of the discharges.

Animals↗