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成年大鼠短暂全脑缺血后视网膜形态、视网膜电图和视觉行为的变化。

Changes in retinal morphology, electroretinogram and visual behavior after transient global ischemia in adult rats.

机构信息

Department of Neurology, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, China.

出版信息

PLoS One. 2013 Jun 11;8(6):e65555. doi: 10.1371/journal.pone.0065555. Print 2013.

Abstract

The retina is a light-sensitive tissue of the central nervous system that is vulnerable to ischemia. The pathological mechanism underlying retinal ischemic injury is not fully understood. The purpose of this study was to investigate structural and functional changes of different types of rat retinal neurons and visual behavior following transient global ischemia. Retinal ischemia was induced using a 4-vessel occlusion model. Compared with the normal group, the number of βIII-tubulin positive retinal ganglion cells and calretinin positive amacrine cells were reduced from 6 h to 48 h following ischemia. The number of recoverin positive cone bipolar cells transiently decreased at 6 h and 12 h after ischemia. However, the fluorescence intensity of rhodopsin positive rod cells and fluorescent peanut agglutinin positive cone cells did not change after reperfusion. An electroretinogram recording showed that the a-wave, b-wave, oscillatory potentials and the photopic negative response were completely lost during ischemia. The amplitudes of the a- and b-waves were partially recovered at 1 h after ischemia, and returned to the control level at 48 h after reperfusion. However, the amplitudes of oscillatory potentials and the photopic negative response were still reduced at 48 h following reperfusion. Visual behavior detection showed there was no significant change in the time spent in the dark chamber between the control and 48 h group, but the distance moved, mean velocity in the black and white chambers and intercompartmental crosses were reduced at 48 h after ischemia. These results indicate that transient global ischemia induces dysfunction of retinal ganglion cells and amacrine cells at molecular and ERG levels. However, transient global ischemia in a 17 minute duration does not appear to affect photoreceptors.

摘要

视网膜是中枢神经系统中对光敏感的组织,容易发生缺血。视网膜缺血性损伤的病理机制尚不完全清楚。本研究旨在探讨短暂性全脑缺血后不同类型大鼠视网膜神经元的结构和功能变化及视觉行为。采用四血管闭塞模型诱导视网膜缺血。与正常组相比,缺血后 6 小时至 48 小时,βIII-微管蛋白阳性视网膜神经节细胞和钙视网膜蛋白阳性无长突细胞数量减少。恢复蛋白阳性视锥双极细胞数量在缺血后 6 小时和 12 小时短暂减少。然而,视紫红质阳性杆状细胞和荧光花生凝集素阳性锥状细胞的荧光强度在再灌注后没有改变。视网膜电图记录显示,在缺血过程中 a 波、b 波、眼动电位和明适应负反应完全丧失。在缺血后 1 小时,a 波和 b 波的振幅部分恢复,在再灌注后 48 小时恢复到对照水平。然而,眼动电位和明适应负反应的振幅在再灌注后 48 小时仍降低。视觉行为检测显示,在对照组和 48 小时组之间,暗室停留时间没有显著变化,但在缺血后 48 小时,黑、白室移动距离、平均速度和隔室交叉减少。这些结果表明,短暂性全脑缺血导致视网膜神经节细胞和无长突细胞在分子和 ERG 水平上功能障碍。然而,持续 17 分钟的短暂性全脑缺血似乎不会影响光感受器。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c306/3679137/7c725d16036c/pone.0065555.g001.jpg

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