COORDINATE CHANGES IN BRAIN ENERGY METABOLISM AND PROTEIN SYNTHESIS

最近的研究已经阐明了体温过高在 脑和其他组织蛋白质合成减少 在服用安非他命之后。脑力减退 热疗后的蛋白质合成与任何 大脑代谢物水平的显著变化，与 除糖原减少外。 对沙土鼠模型的研究已经确定了阈值持续时间 缺血会导致蛋白质合成缺陷。重复 短暂(5分钟)的缺血发作会导致更持久的缺陷 而不是在相似的情况下产生单个5分钟的缺血间隔 条件。反复缺血模型中代谢产物的变化 现在正在被描述为。 最近的合作研究表明，MPP+，活跃的 神经毒素的代谢物MPTP导致显著减少 原代培养小脑颗粒对磷酸肌酸水平的影响 在任何细胞损伤的形态证据之前，细胞神经元。 对这一系统中代谢物变化的进一步评估在 进步。

Recent studies have clarified the central role of hyperthermia in the reduction of protein synthesis in brain and other tissues following amphetamine administration. The decrease in brain protein synthesis after hyperthermia is not associated with any significant alterations in brain metabolite levels, with the exception of a reduction in glycogen. Studies in the gerbil model have determined the threshold duration of ischemia giving rise to protein synthesis deficits. Repeated short (5 min) ischemic episodes result in more lasting deficits than a single 5 min interval of ischemia produced under similar conditions. Metabolite changes in the repeated ischemia model are now being characterized. Recent collaborative studies have shown that MPP+, the active metabolite of the neurotoxin, MPTP, results in a striking reduction in phosphocreatine levels in primary cultures of cerebellar granule cell neurons prior to any morphological evidence of cell injury. Further evaluation of metabolite changes in this system are in progress.