マウスを用いた実験的緑内障モデルの開発とその網膜神経細胞死におけるNMDA受容体ε1サブユニットの関与

概要

論文の詳細を見る
Glaucoma is chronic advance disease of neuronal cell degeneration without inflammation, and final picture of the pathology is retinal ganglion cell death. The machine obstacle theory and the peripheral circulatory obstacle theory have been proposed but the mechanism of glaucoma is still matter of debate. To study the molecular mechanisms of glaucoma, especially roles of the N methyl-D aspatate(NMDA) receptor channel, I developed a experimental mouse glaucoma-tous model. To chronically increase intraocular pressure (IPO) in mouse eyes, I intercepted episcleral veins in two places (medial-superior and lateral-inferior) and stopped the blood-stream. By this treatment, significantly higher IOP which was 55% higher than normal was continued at least 4 weeks. At this time, thickness of the inner reticular layer decreased and the number of retinal ganglion cell also decreased. On the other hand, there was no pathological change in the mice lacking NMDA receptor GluR ε1(NR2A) subunit in which IOP was increased chronically by this method. However, at twelve weeks after treatment, the pathological changes were occur in the GluR ε1 subunit knockout mice which are similar degree of wild type mice. These results suggest that NMDA receptor have a some role in retinal ganglion cell death induced by glaucoma and there are another causal mechanisms.
新潟大学の論文
2004-12-10