STRESS PROTEIN INDUCTION IN GERBIL BRAIN AFTER ISCHEMIA

初步研究证实了主要应激的诱导 (热休克)蛋白，HSP70，短暂性脑缺血后。归纳 还显示了编码泛素的RNAs。免疫细胞化学 HSP70的定位表明，HSP70主要在海马回路中 HSP70可能为神经通路提供了一个标志物 提出了脑缺血后神经元损伤的兴奋毒性机制。 最近的研究结果表明，离子通道拮抗剂 MK-801阻断HSP70诱导，但不能保护HSP70 短暂性脑缺血后死亡的海马神经元。这 为进一步的药理研究提供了基础。 导致基因局部变化的生理机制 脑缺血后的表达。 虽然缺血后HSP70的诱导是神经元的，但高温在 活体反应主要是神经胶质细胞的热休克反应。离体 大鼠小脑星形胶质细胞和颗粒细胞神经元的研究 培养也显示选择性地诱导神经胶质细胞等中的HSP70 培养可能被证明是有用的，以确定分子基础的 体内选择性神经胶质热休克反应。

Initial studies demonstrated the induction of the major stress (heat shock) protein, hsp70, after transient ischemia. Induction of RNAs encoding ubiquitin has also been shown. Immunocytochemical localization of hsp70, largely in hippocampal circuitry, suggests that hsp70 may provide a marker for neuronal pathways mediating proposed excitotoxic mechanisms of neuronal damage after ischemia. Recent results have demonstrated that the ion channel antagonist MK-801 blocks hsp70 induction although it fails to protect hippocampal CA1 neurons which die after transient ischemia. This provides the basis for further pharmacological studies of physiological mechanisms responsible for such local changes in gene expression after ischemia. While postischemic hsp70 induction is neuronal, hyperthermia in vivo results in a largely glial heat shock response. In vitro studies with rat cerebellar astrocytes and granule cell neurons in culture also show selective hsp70 induction in glia and such cultures may prove useful in identifying the molecular basis of the selective glial heat shock response in vivo.