Lack of activated astrocytes in the kindling phenomenon
| Autor: | V. Leviel, J. Brotchi, T. Tanaka |
|---|---|
| Rok vydání: | 1978 |
| Předmět: |
Male
Biological Transport Active Amygdala Basal (phylogenetics) Epilepsy Enzyme activator Developmental Neuroscience Seizures Extracellular medicine Animals Kindling Chemistry Generalized seizure Cobalt medicine.disease Electric Stimulation Rats Cortex (botany) Enzyme Activation medicine.anatomical_structure Neurology Astrocytes Oxidoreductases Neuroglia Oxidation-Reduction Neuroscience |
| Zdroj: | Experimental Neurology. 58:119-125 |
| ISSN: | 0014-4886 |
| DOI: | 10.1016/0014-4886(78)90127-9 |
| Popis: | Proceeding from present hypotheses concerning some causal factors in epilepsy, which suggest the involvement of active ion transport through membranes, we studied the enzyme activities of astrocytes by histochemical methods. Glial cells, probably astrocytes, might act as a buffer to protect neurons against an accumulation of K+ in extracellular spaces. We compared the results obtained with cobalt-induced epilepsy and with the kindling effect in the rat. In the former, we described astrocytes in the cortex characterized by high dehydrogenase activity, which we have called “activated astrocytes”. To obtain the kindling effect, rats fitted with deep bipolar electrodes in the left basal lateral amygdala were stimulated daily to reach a stage of tonic-clonic generalized seizure. Afterward, they were stimulated weekly for various periods (1 to 6 months). In the kindled animals or in the controls, no morphological or histoenzymological anomaly was observed either in the amygdala or in the sensorimotor cortex. No activated astrocytes were found in the kindling effect, which may allow us to conclude that the experimentally decreased threshold of epileptogenic stimulations, without spontaneous seizures, does not lead to modifications in the oxidative metabolism of the astrocytes, contrary to the cobalt model accompanied by spontaneous seizures. |
| Databáze: | OpenAIRE |
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