ALTERATIONS IN TAU IMMUNOSTAINING IN THE RAT HIPPOCAMPUS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA
ALTERATIONS IN TAU IMMUNOSTAINING IN THE RAT HIPPOCAMPUS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA
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DOI：
10.1038/jcbfm.1994.69
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发表时间：
1994-07-01
影响因子：
6.3
通讯作者：
PETTIGREW, LC
中科院分区：
文献类型：
--
作者：
GEDDES, JW;SCHWAB, C;PETTIGREW, LC
先前对沙鼠的研究表明，短暂的短暂性全身缺血后可能会发生细胞骨架破坏和树突微管相关蛋白 MAP2 的丢失。 tau 是一种主要与轴突微管相关的蛋白，尚未在缺血后进行检查。我们在大鼠四血管闭塞模型中缺血 20 分钟后的不同再灌注时间，比较了神经元损伤与 MAP2、tau 和 72-kD 热休克蛋白 (HSP72) 免疫染色的变化。缺血性损伤后 30 分钟至 2 小时，tau 蛋白在整个海马结构的神经细胞体中积累。核周 tau 免疫染色在大多数区域是短暂的，但在多态性肺门神经元中持续存在。与此同时，许多门门神经元目标（齿状回的内分子层）的免疫染色丧失。表现出核周 tau 免疫染色增加的相同神经元群随后表现出 HSP72 免疫反应性的诱导。相反，在神经元死亡之前并没有一致地观察到 MAP2 免疫染色的丧失，并且与 HSP72 的诱导不对应。 tau 免疫染色的改变并不是兴奋性毒性损伤的直接结果，因为海马内注射红藻氨酸不会导致 tau 蛋白在体内积聚，但会导致 MAP2 免疫染色破坏。综上所述，结果表明 tau 蛋白在体内的积累是缺血性损伤的早期、敏感和选择性标志物。
Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, MAP2, may occur after short periods of transient global ischemia. tau, a predominantly axonal microtubule-associated protein, has not been examined following ischemia. We compared neuronal damage with alterations in MAP2, tau, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. tau accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal tau immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunostaining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased tau immunostaining of perikarya later displayed an induction of HSP72 immunoreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered tau immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of tau, but did cause disruption of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of tau is an early, sensitive, and selective marker of ischemic insult.