Production and Glia-Axon Transfer of Heat Shock and Other Glial Proteins

在神经胶质细胞存在的情况下，神经元的功能更好，但由于很难将它们从轴突分子中分离出来，导致这种效应的神经胶质分子鲜为人知。然而，这种分离可以在鱿鱼的巨大轴突中实现，因为它的大小(通常长3-6厘米，直径0.5毫米)。最近，这位研究人员发现，转移到鱿鱼轴突的胶质蛋白中有一种属于热应激蛋白。大多数细胞在急性暴露于代谢压力后都会产生大量的这些蛋白质。随着蛋白质的积累，细胞对潜在的致命压力变得更具抵抗力。胶质细胞-轴突转移应激蛋白的发现代表了神经系统对损伤反应理解的潜在突破，因为它意味着胶质细胞可以向轴突提供蛋白质，以防止轴突在面对创伤时死亡。在鱿鱼巨型轴突中，将利用生化、免疫化学和形态学技术来研究应激蛋白的合成和神经胶质-轴突转移与轴突耐受之间的关系。此外，应激蛋白的转移将与其他胶质蛋白的转移进行比较，以确定是否存在多种胶质细胞-轴突蛋白转移的机制。这项研究项目中描述的工作将展示如何增强神经组织中的应激蛋白反应。这一信息可能提供一种工具，有助于改善中枢神经系统损伤后的功能丧失。潜在地，神经系统创伤后的恢复可以通过刺激应激蛋白的产生或通过给予应激蛋白来改善。更深远的可能性是，通过适当处理应激蛋白反应，神经系统物理创伤后神经元的损失可能会减少。

Neurons function better in the presence of glial cells, but few of the glial molecules responsible for that effect are known because of the difficulty in separating them from axonal molecules. However, that separation can be achieved in the squid giant axon because of its size (typically 3-6 cm long and 0.5 mm in diameter). Recently, this investigator found that one of the glial proteins transferred into the squid axon belongs to the group of heat stress proteins. These proteins are produced in abundance by most cells after acute exposure to metabolic stress. As the proteins accumulate, the cells become more resistant to potentially lethal stress. The discovery of glia-axon transfer of stress proteins represents a potential breakthrough in the understanding of nervous system response to injury because it implies that the glia can provide to the axon proteins designed to keep the axon from dying in the face of trauma. In the squid giant axon, biochemical, immunochemical and morphological techniques will be used to examine the relationship between the synthesis and glia-axon transfer of stress proteins and axonal stress tolerance. Additionally, stress proteins transfer will be compared to the transfer of other glial proteins to determine if there are multiple mechanisms of glia-axon protein transfer. The work described in this research project will show how the stress protein response in nerve tissue can be enhanced. This information may provide a tool that can help to ameliorate the loss of function after central nervous system injury. Potentially, recovery after nervous system trauma could be improved by stimulation of the production of stress proteins or by administering stress proteins. More far-reaching is the possibility that the loss of neurons after physical trauma to the nervous system could be reduced by proper manipulation of the stress protein response.