Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan.
Neurosci Lett. 2010 Nov 12;485(1):55-9. doi: 10.1016/j.neulet.2010.08.061. Epub 2010 Aug 27.
Retinal ischemia-reperfusion causes capillary degeneration but the mechanisms of damage are not well understood. The NMDA receptor plays an important role in neuronal damage after ischemia-reperfusion. Therefore, we determined whether retinal blood vessels are damaged structurally and functionally in a rat model of retinal degeneration induced by NMDA. At 7 days after a single intravitreal injection of NMDA (200nmol) into the eye, loss of retinal ganglion cells and thinning of the inner plexiform layer were observed. Endothelial cells disappeared in some regressing vessels and empty basement membrane sleeves were left as remnants of the vessels. The number of basement membrane sleeves was increased in the NMDA-treated retina and non-perfused vessels were found in the injured retina. These results indicate that retinal blood vessels are damaged in the NMDA-induced retinal degeneration model. Neuronal cells may play a role in maintaining normal structure and function of the vasculature in the retina.
视网膜缺血再灌注可导致毛细血管退化，但损伤机制尚不清楚。NMDA 受体在缺血再灌注后神经元损伤中发挥重要作用。因此，我们在 NMDA 诱导的大鼠视网膜变性模型中确定视网膜血管是否在结构和功能上受到损伤。在单次玻璃体内注射 NMDA（200nmol）后 7 天，观察到视网膜神经节细胞丢失和内丛状层变薄。在一些退化的血管中，内皮细胞消失，留下空的基底膜套管作为血管的残留物。NMDA 处理的视网膜中基底膜套管的数量增加，并且在损伤的视网膜中发现无灌注的血管。这些结果表明，NMDA 诱导的视网膜变性模型中视网膜血管受损。神经元细胞可能在维持视网膜血管的正常结构和功能中发挥作用。
