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首页> 外文期刊>Brain research >Tyrosine kinase A but not phosphacan/protein tyrosine phosphatase-zeta/beta immunoreactivity and protein level changes in neurons and astrocytes in the gerbil hippocampus proper after transient forebrain ischemia.
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Tyrosine kinase A but not phosphacan/protein tyrosine phosphatase-zeta/beta immunoreactivity and protein level changes in neurons and astrocytes in the gerbil hippocampus proper after transient forebrain ischemia.

机译:短暂性前脑缺血后,沙土鼠海马中神经元和星形胶质细胞中的酪氨酸激酶A而非磷酸/蛋白质酪氨酸磷酸酶-zeta /β免疫反应性和蛋白质水平变化。

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摘要

In the present study, ischemia-related changes in tyrosine kinase A (trkA) and phosphacan/protein tyrosine phosphatase-zeta/beta (PTP-zeta/beta) immunoreactivities and protein contents were examined in the hippocampus proper after transient forebrain ischemia for 5 min in a gerbil model. Our investigations showed that ischemia-induced changes occurred in trkA immunoreactivity in the hippocampal CA1 region, but not in the CA2/3 region of the hippocampus proper. In the sham-operated group, trkA immunoreactivity was barely detectable. trkA immunoreactivity increased from 30 min after ischemia and peaked at 12 h. Four days after ischemic insult, trkA immunoreactivity was observed in GFAP-immunoreactive astrocytes in the strata oriens and radiatum. In addition, we found that ischemia-related changes in trkA protein content were similar to immunohistochemical changes. On the other hand, PTP-zeta/beta immunoreactivities in the hippocampus proper were unaltered by forebrain ischemia. These results suggest thatchronological changes of trkA after transient forebrain ischemia may be associated with an ischemic damage compensatory mechanism in CA1 pyramidal cells.
机译:在本研究中,短暂性前脑缺血5分钟后,检查海马中与酪氨酸激酶A(trkA)和磷酸/蛋白酪氨酸磷酸酶-zeta / beta(PTP-zeta / beta)免疫反应性和蛋白质含量相关的缺血相关变化在沙鼠模型中我们的研究表明,缺血诱导的海马CA1区trkA免疫反应性发生了变化,但在海马CA2 / 3区却没有。在假手术组中,几乎未检测到trkA免疫反应性。 trkA免疫反应性从缺血后30分钟开始增加,并在12 h达到峰值。缺血性损伤后四天,在层和辐射层的GFAP免疫反应星形胶质细胞中观察到trkA免疫反应性。此外,我们发现与缺血相关的trkA蛋白含量变化与免疫组化变化相似。另一方面,前脑缺血不会改变海马体中的PTP-zeta /β免疫反应性。这些结果表明短暂性前脑缺血后trkA的时间变化可能与CA1锥体细胞的缺血性损害补偿机制有关。

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