Severity of middle cerebral artery occlusion determines retinal deficits in rats.
Severity of middle cerebral artery occlusion determines retinal deficits in rats.
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DOI：
10.1016/j.expneurol.2014.02.005
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发表时间：
2014-04
影响因子：
5.3
通讯作者：
Stein, Donald G.
中科院分区：
文献类型：
--
作者：
Allen, Rachael S.;Sayeed, Iqbal;Cale, Heather A.;Morrison, Katherine C.;Boatright, Jeffrey H.;Pardue, Machelle T.;Stein, Donald G.
线栓法大脑中动脉闭塞(MCAO)是研究啮齿类动物脑缺血的常用模型。由于眼动脉靠近大脑中动脉，大脑中动脉阻塞两条动脉，导致大脑和视网膜缺血。虽然之前的研究显示MCAO后48小时出现视网膜功能障碍，但我们调查了这些视网膜功能障碍是否会持续到9天，以及它们是否与中枢神经功能障碍相关。大鼠接受90分钟的短暂大脑中动脉阻塞，然后在第2天和第9天进行视网膜电描记术以评估视网膜功能。用甲酚紫染色、胶质纤维酸性蛋白(GFAP)和谷氨酰胺合成酶免疫组织化学染色和TUNEL染色评价视网膜损伤。2天后，大鼠表现出行为缺陷，用与脑梗塞面积和视网膜功能相关的神经评分进行评估。手术后两天，中度MCAO(神经评分5分)大鼠视网膜电信号潜伏期延迟，而重度MCAO(神经评分≥5)大鼠视网膜电信号波幅降低。重度和中度动物MCAO后3d，Müler细胞谷氨酰胺合成酶表达上调，而重度动物MCAO视网膜神经节细胞死亡。在MCAO后第9天，中度动物的谷氨酰胺合成酶标记和视网膜电信号均恢复到正常水平。早期视网膜功能缺陷与行为缺陷相关。然而，视网膜功能的下降是一过性的，只有在严重的缺血时才能观察到选择性的视网膜细胞丢失，这表明视网膜比大脑更不容易受到MCAO的影响。MCAO引起的暂时性视网膜损伤可能是由于缺血引起的细胞外谷氨酸的增加，这损害了信号传导，但在MCAO后9天就消失了。
Middle cerebral artery occlusion (MCAO) using the intraluminal suture technique is a common model used to study cerebral ischemia in rodents. Due to the proximity of the ophthalmic artery to the middle cerebral artery, MCAO blocks both arteries, causing both cerebral and retinal ischemia. While previous studies have shown retinal dysfunction at 48 hours post-MCAO, we investigated whether these retinal function deficits persist until 9 days and whether they correlate with central neurological deficits. Rats received 90 minutes of transient MCAO followed by electroretinography at 2 and 9 days to assess retinal function. Retinal damage was assessed with cresyl violet staining, immunohistochemistry for glial fibrillary acidic protein (GFAP) and glutamine synthetase, and TUNEL staining. Rats showed behavioral deficits as assessed with neuroscore that correlated with cerebral infarct size and retinal function at 2 days. Two days after surgery, rats with moderate MCAO (neuroscore < 5) exhibited delays in electroretinogram implicit time, while rats with severe MCAO (neuroscore ≥ 5) exhibited reductions in amplitude. Glutamine synthetase was upregulated in Müller cells 3 days after MCAO in both severe and moderate animals, however, retinal ganglion cell death was only observed in MCAO retinas from severe animals. By 9 days after MCAO, both glutamine synthetase labeling and electroretinograms had returned to normal levels in moderate animals. Early retinal function deficits correlated with behavioral deficits. However, retinal function decreases were transient and selective retinal cell loss was observed only with severe ischemia, suggesting that the retina is less susceptible to MCAO than the brain. Temporary retinal deficits caused by MCAO are likely due to ischemia-induced increases in extracellular glutamate that impair signal conduction, but resolve by 9 days after MCAO.
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影响因子：
11.1
作者：
FALKE, P;ABELA, BM;STAVENOW, L
通讯作者：
STAVENOW, L
影响因子：
4.8
作者：
BEAL, MF
通讯作者：
BEAL, MF
影响因子：
6.3
作者：
HILLERED, L;HALLSTROM, A;UNGERSTEDT, U
通讯作者：
UNGERSTEDT, U
影响因子：
1.9
作者：
HOOD, DC;BIRCH, DG
通讯作者：
BIRCH, DG
DOI：
10.1051/rnd:2006033
发表时间：
2006-09-01
期刊：
REPRODUCTION NUTRITION DEVELOPMENT
影响因子：
--
作者：
Acar, Niyazi;Bonhomme, Brigitte;Chardigny, Jean-Michel
通讯作者：
Chardigny, Jean-Michel