[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.

[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.

[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.

[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.

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.

[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.

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.

[Experimental study of a rostro-caudal systemization in the inferior olivary complex].

Injection of 3-acetylpyridine at a LD50 dose to albino rats produces in a few days the destruction of olivary neurons. But the caudal part of the olivary complex, particularly accessory olives, escapes the destruction by this antimetabolite of nicotinamide. Nicotinamide protects olives agains 3-acetylpyridine.

[Evolution of the astroglial reaction in the pyramidal pathway after injury of the rat motor cortex].

Investigation of astrocytes in the pyramidal tract of the rat 2 to 100 days after a lesion of the motor cortex indicates that the glial reaction, with increase in size of astrocytes and in affinity for Cajal's gold-sublimate, begins at the lesion and extends to the distal segments of the spinal cord. But this reaction recedes and disappears in lumbar and dorsal cord about 70 days after the operation. It persists in the cervical cord and in the brain.

[Location and somatotopic organization of visceromotor, motor and sensory columns of the cranial nerves].

The author describes the origins and endings of sensory, motor and visceromotor fibers of cranial nerves, special senses excluded. He gives cytological and cytochemical characteristics of neurons and relates experimental and pathological data. References are mostly limited to recent papers.