STRESS PROTEIN INDUCTION IN GERBIL BRAIN AFTER ISCHEMIA

编码70 kDa主要热源的mRNA的原位杂交研究 休克/应激蛋白hsp70已证明其在 短暂性全脑缺血后脆弱的海马神经元。这些 细胞还会经历蛋白质合成的持久损害，这可能 促成了这种超感应现象。原癌基因c-fos， 仅显示瞬时增加的表达，但有分布 与再灌流早期hsp70m RNA的表达水平一致。这些 结果提示，相关的信号转导机制可能是 负责这些RNAs的诱导，并支持 HSP70O杂交法作为持续性疾病某些方面的可能指标 神经元激活。缺血2分钟的阈值已经被 建立了在沙土鼠体内诱导hsp7O的方法。 热疗后观察到一种更复杂的诱导模式， 免疫反应蛋白主要分布于神经胶质细胞和血管 但hsp7O mRNA在神经元中的叠加定位 体温严重过高。 未来研究的主要方向是利用hsp70的变化， C-fos和其他mRNAs和蛋白质作为工具识别准确的 个体细胞类型对病理生理学进化的贡献 在不同的大脑侮辱之后，并阐明特定的信号 涉及的转导机制。

In situ hybridization studies of mRNA encoding the major 70 kDa heat shock/stress protein, hsp7O, have demonstrated its prolonged expression in vulnerable hippocampal CAl neurons after transient global ischemia. These cells also experience a lasting impairment of protein synthesis that may contribute to such a superinduction phenomenon. The proto-oncogene, c-fos, shows only transiently increased expression but with a distribution identical to that of hsp7O mRNA at early recirculation intervals. These results suggest that related signal transduction mechanisms may be responsible for the induction of these RNAs, and support the utility of hsp7O hybridization as a possible indicator of some aspect of persistent neuronal activation. A threshold of 2 minutes ischemia has been established for induction of hsp7O in the gerbil. A more complex pattern of induction is observed after hyperthermia, with a predominantly glial and vascular distribution of immunoreactive protein but a superimposed neuronal localization of hsp7O MRNA during increasingly severe hyperthermia. The major direction of future studies is to utilize changes in hsp7O, c-fos and other mRNAs and proteins as tools for identifying the precise contributions of individual cell types to the evolution of pathophysiology following diverse brain insults, and to elucidate the specific signal transduction mechanisms involved.