Soriano M A, Tortosa A, Planas A M, Rodriguez-Farré E, Ferrer I
Unitat de Neuropatologia, Serivei d'Anatomia Patològica, Hospital Princeps d'Espanya, Universitat de Barcelona, Spain.
Brain Res. 1994 Aug 8;653(1-2):191-8. doi: 10.1016/0006-8993(94)90389-1.
The effects of a 20-min transient episode of forebrain ischemia on the induction of HSP70 mRNA and protein, and the histopathological outcome in the hippocampus of the developing gerbil, were examined at postnatal days (P) 7, 15, 21 and 30 and in adulthood. 4 days after the ischemic episode, P7 gerbils did not show apparent histological abnormalities; however, from P15 onwards, ischemia resulted in necrosis in selected areas of the hippocampus. At P15 and P21, necrosis was observed in the base of the granular cell layer of the dentate gyrus and in the CA3 pyramidal cell layer, whereas at P30 and adult necrosis was apparent in the CA1 pyramidal cell layer. HSP70 mRNA induction was not found in ischemic P7 and P15 gerbils while, from P21 onwards, induction was observed in the dentate gyrus and CA1 pyramidal cell layer. In addition, at P30 and adult, HSP70 mRNA expression was also seen in CA3 pyramidal cell layer. Induction of HSP70 immunoreactivity was not seen at P7 but, from P15 onwards, ischemia induced HSP70 immunoreactivity in different areas: in dentate gyrus granular and molecular layers, from P15 onwards; in CA1 pyramidal cell layer, from P21 onwards; and in CA3 pyramidal cell layer, from P30 onwards. Results show selective age-dependent patterns of vulnerability to ischemia in the gerbil hippocampus which, overall, were not well-correlated to the corresponding HSP70 mRNA and protein induction patterns.
研究了20分钟短暂性前脑缺血对新生沙鼠海马中HSP70 mRNA和蛋白诱导以及组织病理学结果的影响，观察时间点为出生后第（P）7、15、21和30天以及成年期。缺血发作4天后，P7沙鼠未表现出明显的组织学异常；然而，从P15开始，缺血导致海马特定区域出现坏死。在P15和P21时，在齿状回颗粒细胞层底部和CA3锥体细胞层观察到坏死，而在P30和成年期，CA1锥体细胞层出现明显坏死。在缺血的P7和P15沙鼠中未发现HSP70 mRNA诱导，而从P21开始，在齿状回和CA1锥体细胞层观察到诱导。此外，在P30和成年期，CA3锥体细胞层也可见HSP70 mRNA表达。P7时未观察到HSP70免疫反应性诱导，但从P15开始，缺血在不同区域诱导了HSP70免疫反应性：从P15开始在齿状回颗粒层和分子层；从P21开始在CA1锥体细胞层；从P30开始在CA3锥体细胞层。结果显示沙鼠海马对缺血的易损性存在年龄依赖性的选择性模式，总体而言，这些模式与相应的HSP70 mRNA和蛋白诱导模式相关性不佳。
