Moroni F, Lombardi G, Pellegrini-Faussone S, Moroni F
Ophthalmology Clinic, University of Florence, Italy.
Vision Res. 1993 Sep;33(14):1887-91. doi: 10.1016/0042-6989(93)90016-p.
The effects of ischemia-induced retinal damage were quantitatively evaluated in rats with the aim of obtaining a suitable model to study the pathogenesis of the loss of retinal neurons after ischemic episodes. Anaesthetized rats were injected with 80 mg/kg i.v. of the fluorescein rose bengal dye and one eye was exposed to cold light for different periods (from 5 to 30 min). The animals were sacrificed at different times (1 and 4 hr; 2 and 7 days) after the lesion and the photochemically-induced damage was evaluated. The damaged retinae appeared thicker, numerous neurons of the inner nuclear layers showed swelling of the perinuclear cytoplasm and the retinal vessels were enlarged. The activity of choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD), two marker enzymes of the GABAergic and cholinergic neurons, significantly decreased, indicating a degeneration of GABAergic and cholinergic amacrine cells.
为了获得一个合适的模型来研究缺血发作后视网膜神经元丧失的发病机制,对大鼠缺血性视网膜损伤的影响进行了定量评估。将麻醉的大鼠静脉注射80mg/kg的荧光素孟加拉红染料,一只眼睛暴露于冷光下不同时间(5至30分钟)。在损伤后的不同时间(1和4小时;2和7天)处死动物,并评估光化学诱导的损伤。受损的视网膜看起来更厚,内核层的许多神经元显示核周细胞质肿胀,视网膜血管扩张。胆碱乙酰转移酶(ChAT)和谷氨酸脱羧酶(GAD)这两种GABA能和胆碱能神经元的标记酶的活性显著降低,表明GABA能和胆碱能无长突细胞发生退化。