Transient ischemia of the retina results in altered retrograde axoplasmic transport:: Neuroprotection with brimonidine
Transient ischemia of the retina results in altered retrograde axoplasmic transport:: Neuroprotection with brimonidine
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DOI：
10.1006/exnr.2002.8043
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发表时间：
2002-12-01
影响因子：
5.3
通讯作者：
Vidal-Sanz, M
中科院分区：
文献类型：
--
作者：
López-Herrera, MPL;Mayor-Torroglosa, S;Vidal-Sanz, M
在成年大鼠中，我们诱导了视网膜缺血，并研究了神经节细胞中的逆行轴突运输。在缺血前1小时，动物左眼接受两滴5-穆尔盐水或0.5%溴莫尼定（BMD）。视网膜缺血引起短暂结扎的左眼血管90分钟。缺血后1小时或1周，荧光金（FG）应用于两个上级丘，动物处理后1周FG应用，FG标记的视网膜神经节细胞（RGC）密度估计在右侧对照和左侧实验视网膜。在生理盐水预处理的动物的左侧视网膜中，RGC密度在缺血后7或14天分别降低至其右侧对照视网膜中发现的密度的39或30%。因为在先前的类似研究中，在缺血前7天应用FG，缺血后7天和14天FG标记的RGC的百分比分别为54%和48%，这表明在一些存活的RGC中逆行轴突运输受损。这在另一组大鼠中得到证实，其中在缺血前3周将1，1 ′-双十八烷基-3，3，3 ′，3 ′-四甲基吲哚羰花青高氯酸盐应用于两个SCi，并在缺血后9天和安乐死前5天将FG应用于眶内切割的视神经。在BMD预处理的动物的左侧视网膜中，RGC密度在缺血后7或14天达到RGC群体的90%，并且与在其对侧非缺血性视网膜中获得的密度相当。视网膜缺血导致R损失并诱导一定比例的存活RGC的逆行轴突运输改变。BMD挽救缺血诱导的细胞死亡的RGCs，并保留逆行轴突运输存活的RGCs。(C)2002 Elsevier Science（美国）。
In adult rats we have induced retinal ischemia and investigated retrograde axonal transport in ganglion cells. The animals received in their left eyes, 1 h prior to ischemia, two 5-mul drops of saline or 0.5% brimonidine (BMD). Retinal ischemia was induced by transient ligature of the left ophthalmic vessels for 90 min. One hour or 1 week after ischemia, Fluorogold (FG) was applied to both superior colliculi, the animals were processed 1 week after FG application, and FG-labeled retinal ganglion cell (RGC) densities were estimated in the right control and left experimental retinas. In the left retinas of the saline-pretreated animals, RGC densities diminished to 39 or 30% of the densities found in their right control retinas, 7 or 14 days after ischemia, respectively. Because in a previous similar study in which FG was applied 7 days before ischemia, the percentages of FG-labeled RGCs were 54 and 48%, 7 and 14 days after ischemia, respectively, this suggests that retrograde axonal transport was impaired in some surviving RGCs. This was confirmed in an additional group of rats in which 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate was applied to both SCi 3 weeks before ischemia, and FG was applied to the intraorbitally cut optic nerve 9 days after ischemia and 5 days before euthanization. In the left retinas of the BMD-pretreated animals, RGC densities amounted to 90% of the RGC population 7 or 14 days after ischemia and were comparable to those obtained in their contralateral nonischemic retinas. Retinal ischemia causes R loss and induces alterations of retrograde axonal transport in a proportion of surviving RGCs. BMD rescues RGCs from ischemia-induced cell death and preserves retrograde axonal transport in surviving RGCs. (C) 2002 Elsevier Science (USA).