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.
