Abstracts

RATIONALE: We developed a new rodent model of focal cortical dysplasia (FCD). The characteristics of this model were analyzed and its clinical application was discussed.
METHODS: Neonatal Wistar rats (P 0-2) were anesthetized with 2.0% halothane. A small skull hole was made with a percutaneous prick of 27G needle. The prick point was 2mm anterior, 3mm lateral to the bregma and 3mm deep from the skin. Kainic acid (KA) was dissolved in a phosphate buffer to prepare 1.0mg/ml KA solution. A stainless-steel injection needle was inserted using this small hole and 0.5[mu]l of KA solution was injected into the cerebral cortex. One or two months following the KA injection, the animals were sacrificed and their brains were removed. Coronal sections of the brain were stained with H-E, cresyl violet, NSE and GFAP. The histopathological findings were examined.
RESULTS: Tonic-clonic seizures were induced by an intracortical injection of KA in all animals. The seizures lasted for 24 hours. The most of them tolerated and survived from the seizures. The animals were grown up for 2 months without experience of spontaneous seizures. Histopathologically, normal lamination of cortical neurons was destructed around the KA-injected region, and some atypical neurons were found around the lesion with dislamination of the cortical layers. The histopathological changes detected were almost the same in the animals of one month and two months after KA injection.
CONCLUSIONS: A new model of focal cortical dysplasia was induced by local KA injection in neonatal rats. The neuronal hyperexcitation and toxicity of KA modified normal cortical organization in a neonatal period. Although long-term observation is required to confirm whether spontaneous seizure will develop or not, this model may be useful to study the epileptogenesity of FCD.