深部前梨状葉皮質の間欠的電気刺激によるてんかん発作重積モデル

Hippocampal damage induced by status epilepticus (SE) has been suggested as the developmental pathway of temporal lobe epilepsy. We developed an experimental model of SE induced by massed electrical stimulations into the deep prepiriform cortex. Stimulations under aminophylline pretreatment more effectively induced SE than those in the absence of aminophylline. Most SE episodes included secondary generalized seizures. Cresyl violet staining indicated neuronal degeneration in CA1 and CA3, 1-2 weeks after the SE. Mild neuronal loss was observed 8 weeks after the SE, although there were no obvious histological changes in the hilus. Immunoreactivity for GluR1, a subunit of the AMPA receptors, was reduced in CA3 and the hilus starting 1 week after SE, indicating a discrepancy between the distributions of neuronal damage and the GluR1 decrement. The present model serves as a useful model of SE. Further improvement of this method will make it an effective tool for understanding the developmental process of temporal lobe epilepsy.

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