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J Korean Child Neurol Soc. 2001 Oct;9(2):310-319. Korean. Original Article.
Kim JM , Lee CW , Oh KS , Park ST .
Department of Pediatrics, School of Medicine, Wonkwang University, Iksan, Korea.
Department of Anatomy, School of Medicine, Wonkwang University, Iksan, Korea.
Abstract

PURPOSE: Our study was an experimental model for the mechanism of cortical dysplasia. We examined the changes of neuronal cells and glial cells by intrauterine irradiation. This paper will elucidate the effect of these changes on the development of cortical dysplasia. METHODS: The cytotoxic effect of irradiation was examined by viability and numbers in cerebral cortical neurons and glial cells, which were derived from a mouse exposed to 225 cGy of gamma-irradiation on embryonic day 17. In addition, the protective effect of an inhibitor of intracellular calcium release, dantrolene sodium(DS), on irradiation-induced neurotoxicity was examined after DS(10 mg/kg) was administrated via intraperitoneal injection after intrauterine irradiation. RESULTS: 1) Irradiation induced the decrement of the cell number and cell viability of cerebral cortical neurons in the developing stages. 2) The number of glial cells in the mouse treated with intrauterine irradiation was increased in E20-P4 stages compared with the control group, but there was no difference in cell viability. 3) The glial fibrillary acidic protein(GFAP)-positive cells were seen in developing stages (E20-P4). 4) In the protective effect from neuronal cell death by intrauterine irradiation, DS attenuated cell death by an increase of neuronal cells. CONCLUSION: From these results, it is suggested that intrauterine irradiation has the neurotoxic effect as neuronal cell death and induced glial cell proliferation. A selective inhibitor of intracellular calcium release such as DS is effective in protecting neuronal cell death induced by irradiation of the intrauterine period. Cortical dysplasia induced by intrauterine irradiation may be involved in neuronal cell death and the hyperproliferation of glial cells. Intracellular calcium influx may contribute to the pathogenesis of irradiation-induced neuronal cell death.

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