ETHANOL AND NERVOUS SYSTEM DEGENERATION

超过60%的慢性酗酒者会出现脑损伤。原因和 然而，这种损伤的病理生理学还知之甚少。这个 我们研究的总体目标是评估导致 酒精诱导的实验性神经系统退行性变 动物。乙醇已被证明可以从细胞内释放钙。 储存地点。细胞内钙离子的增加激活了蛋白水解酶 细胞骨架蛋白的蛋白质分解。存在这样可能性，即一些 酒精诱导的退行性变的影响可能是激活 这些蛋白酶。为了研究细胞内钙离子的作用 在神经元变性过程中，我们使用了鱿鱼巨型轴突作为模型 系统。使用这种制剂的优点是，酶和 底物可以从巨大的轴突中以高产量挤出，从而避免 制剂受到非轴突酶的污染，可能会成为 在整个组织的均质化过程中非特异性地附着。 第二，轴浆和轴浆中存在的酶活性和底物。 制备方法可以与存在的活动和底物进行比较 星状神经节的区域，它包含了 巨大的轴突。在鱿鱼的轴突和细胞体中，我们已经确定了一些 钙激活蛋白降解后的免疫反应降解产物。 结果表明，胞浆内游离钙的升高可能 导致蛋白质的分解。

Brain damage occurs in over 60% of chronic alcoholics. The causes and pathophysiology of this damage, however, are poorly understood. The general goal of our research has been to evaluate the factors that lead to alcohol-induced degeneration of the nervous system in experimental animals. Ethanol has been shown to release calcium from intracellular storage sites. The increase in cytosolic calcium activates proteases cause proteolysis of cytoskeletal proteins. The possibility exist that some of the effects of alcohol-induced degeneration may be to the activation of these proteases. In order to investigate the role of intracellular calcium during neuronal degeneration we have used the squid giant axon as a model system. The advantages of using this preparation are that the enzyme and substrates can be extruded in high yield from the giant axon, thus avoiding contamination of the preparation with nonaxonal enzymes, which may become nonspecifically attached during the homogenization of whole tissue. Second, enzyme activities and substrates present in axoplasm and axoplasmic preparations can be compared with the activities and substrates present in the region of the stellite ganglion, which contains the cell bodies of the giant axon. In the squid axon and cell body we have identified a number of immunoreactive degradation products after calcium-activated proteolysis. The results suggest that an elevation of cytosolic ionized calcium may result in a breakdown of proteins.