目的: 探讨低强度激光致视网膜损伤效应的可能机制。方法: 建立氦氖激光的大鼠眼损伤模型, 通过免疫组化和原位杂交等方法, 观察低强度激光照射后视网膜细胞中谷氨酸受体(NMDAR)的表达变化。结果: 免疫组化和原位杂交的结果显示在正常视网膜组织未见或仅见有NMDAR的轻微表达, 而在激光照射后6 h其表达开始增加, 并于照后3 d达到高峰, 7 d后开始逐渐下降, 这与视网膜激光损伤后感光神经元的凋亡在时相上呈现出一致性。结论: 低强度激光照射后视网膜局部谷氨酸的过度释放及NMDAR受体的高表达可能是感光神经元损伤凋亡的重要机制。

Objective: This study is proposed to investigate the possible mechanism of low power laser-induced retina injury. Methods: Wistar rats were irradiated continually with low power He-Ne laser for 15 mins. At different intervals after laser exposure, the effects of low power laser irradiation on the expression of glutamate receptor(NMDAR)in the rar retina were determined by immunohistochemistry(IHC)and in situ hybridization (ISH). Results: There was only trace expression of NMDAR in the normal retinas．After laser irradiation the NMDAR expression began to increase at 6h, amounted to the peak at 3d, and gradually decreased at 7 d and the fluctuations of NMDAR expression coincident to the phase of photoreceptor apoptosis. Conclusion: Induced high expressions of NMDAR is one of the possible mechanisms by which low power laser irradiation caused experimental injury of rats retina．