COORDINATE CHANGES IN BRAIN ENERGY METABOLISM AND PROTEIN SYNTHESIS

大脑能量代谢和蛋白质合成的变化已经被 其特征在于沙鼠短暂的双侧缺血。 体外翻译产物的二维凝胶分析 电泳已经证明了主要哺乳动物 应激诱导或热休克蛋白（hsp 70），在再灌注过程中 缺血5 min后。 热休克蛋白70的表达逐渐增加 再循环后，在约8小时达到最大值 再循环，并在24小时内恢复到接近控制水平。相反， 所有其他单独的蛋白质的合成都急剧下降 缺血后，并返回到对照水平， 总掺入活性的恢复。 这种短暂的诱导 热休克蛋白70类似于经典的热休克反应， 系统，尽管HSP 70从未成为主要的翻译产品。 在对照组的制备物中检测到低水平的HSP 70合成 在对照脑的银染凝胶中可以发现该蛋白 proteins. HSP 70的初步免疫组织化学定位表明 它存在于基本上所有的神经元细胞体中。 初步的放射免疫测定数据表明， 阿片肽，强啡肽A，在沙鼠大脑半球的1和 缺血5分钟后24小时。 β-内啡肽和甲硫脑啡肽水平 不受缺血的影响，尽管这些实验中使用的沙鼠种群 关于β-内啡肽， 大脑的水平。 这些观察结果可能与冲突有关。 阿片拮抗剂对该动物中风症状的影响的报告 模型

Changes in brain energy metabolism and protein synthesis have been characterized following transient bilateral ischemia in the gerbil. Analysis of in vitro translation products by two dimensional gel electrophoresis has demonstrated the induction of the major mammalian stress-induced or heat shock protein, (hsp 70), during recifulation following 5 min ischemis. Expression of hsp 70 increases gradually following recirculation, reaching a maximum at approximately 8 hr recirculation, and returns to near control levels by 24 hr. In contrast, the synthesis of all other individual proteins exzamined fell dramatically following ischemia and returned to control levels in parallel with the recovery of overall incorporation activity. This transient induction of hsp 70 resembles the classical heat-shock response defined on other systems, although at no time does hsp 70 become a major translation product. A low level of hsp 70 synthesis is detected in preparations from control brain, and the protein can be found in silver stained gels of control brain proteins. Preliminary immunohistochemical localization of hsp 70 indicates its presence in essentially all neuronal cell bodies. Preliminary radioimmunoassay data have demonstrated a 30% depletion of the opiate peptide, dynorphin A, in gerbil cerebal hemispheres between 1 and 24 hr following 5 min ishchemia. Beta-endorphin and met-enkephalin levels were not affected by ischemia, although the gerbil population used in these studies appears to be quite heterogenous with regard to beta-endorphin levels in brain. These observations may be relevant to the conflicting reports of effects of opiate antagonists on stroke symptoms in this animal model.