Functional changes mediated by high-intraocular pressure-induced optic nerve damage in lateral geniculate body and visual cortex of monkeys.

1)研究NMDA诱导的小鼠视网膜损伤后外侧膝状体(LGN)内随时间变化的局灶性改变。注射NMDA后1d即可观察到视网膜损伤。注射NMDA后7d，对侧视束萎缩。在对侧LGN背侧(d-LGN)和对侧腹侧LGN-1(vLGN-1)，神经元数量分别在注射NMDA后90d和180d开始减少，神经元大小分别在注射NMDA后30d和7d开始缩小。在神经元变性过程中，对侧dLGN和vLGN-1的胶质纤维酸性蛋白(GFAP)和脑源性神经营养因子(BDNF)的表达增加，部分GFAP阳性的星形胶质细胞也表达BDNF。注射NMDA后，视网膜化通路(从视网膜到LGN)发生了时间依赖性的局灶性改变，LGN的损伤程度是区域依赖性的。在受影响的LGN区域GFAP和BDNF的表达增加可能在该核团的逆行细胞死亡机制中起一定作用。2)HRT和GDX显示，随着眼压的升高，猴眼视盘形态和RNFL厚度随时间发生变化。HRT(边缘和杯状)参数与组织学RNFL厚度有很好的相关性，且相关性显著。

1) The purpose was to investigate time-dependent, exofocal alterations in the lateral geniculate nucleus (LGN) following NMDA-induced retinal damage in mice. Retinal damage was noted at 1 day after NMDA injection. At 7 days after NMDA injection, atrophy of the optic tract was observed on the contralateral side. In the contralateral dorsal LGN (d-LGN) and contralateral ventral LGN-lateral (vLGN-1), neurons were first decreased in number at 90 and 180 days, respectively, after NMDA injection, and neuronal cell-size was first decreased at 30 and 7 days, respectively, after NMDA injection. During this neuronal degeneration, expressions of glial fibrillary acidic protein (GFAP) and brain-derived neurotrophic factor (BDNF) were increased in the contralateral dLGN and vLGN-1, with some GFAP-positive astroglial cells also exhibiting BDNF. After NMDA injection, time-dependent, exofocal alterations occurred along the retinogeniculate pathway (from retina to LGN), and the degree of damage in LGN was region-dependent. Increased expressions of GFAP and BDNF in the affected LGN regions may play some roles in the retrograde cell-death mechanism in this nucleus.2) Alongside the IOP elevation, time-related changes in optic disc topography and RNFL thickness were demonstrated in monkey eyes using HRT and GDx. HRT (rim and cup) parameters showed good correlations with histological RNFL thickness, and significant interrelations.