Hwang In Koo, Lee Kyoung Youl, Yoo Ki-Yeon, Kim Duk Soo, Lee Nam Seob, Jeong Young-Gil, Kang Tae-Cheon, Han Byoung Hee, Kim Jong Sung, Won Moo Ho
Department of Anatomy, College of Medicine, Hallym University, Chunchon 200-702, South Korea.
Brain Res. 2005 Mar 2;1036(1-2):35-41. doi: 10.1016/j.brainres.2004.12.037.
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 that chronological changes of trkA after transient forebrain ischemia may be associated with an ischemic damage compensatory mechanism in CA1 pyramidal cells.
在本研究中，我们在沙土鼠模型中对前脑进行5分钟的短暂缺血后，检测了海马体中酪氨酸激酶A（trkA）和磷酸聚糖/蛋白酪氨酸磷酸酶-ζ/β（PTP-ζ/β）免疫反应性及蛋白含量的缺血相关变化。我们的研究表明，海马CA1区的trkA免疫反应性出现了缺血诱导的变化，但在海马体本身的CA2/3区未出现。在假手术组中，几乎检测不到trkA免疫反应性。trkA免疫反应性在缺血后30分钟开始增加，并在12小时达到峰值。缺血损伤4天后，在海马体原层和辐射层中GFAP免疫反应性星形胶质细胞中观察到trkA免疫反应性。此外，我们发现trkA蛋白含量的缺血相关变化与免疫组化变化相似。另一方面，前脑缺血并未改变海马体本身的PTP-ζ/β免疫反应性。这些结果表明，短暂前脑缺血后trkA的时间变化可能与CA1锥体细胞的缺血损伤代偿机制有关。
