The structure and electrophysiological characteristics of central spinal axons will be determined during successive stages of the inflammatory response that follows spinal cord contusion injury, in cats. The time-course and mechanism of dysfunction in surviving axons will be investigated, using intracellular microelectrode recording and current-injection in an in vitro preparation of spinal cord. The quantitative extent of axonal survival and myelination will be examined with light- and electron-microscopy, for comparison with physiological recordings in the same tissue. The myelination and electrophysiology of selected individual axons will be correlated by electrophoretic injection of horseradish peroxidase at the time of recording, and subsequent processing for microscopy. The time-course and extent of phagocytic infiltration of the tissue, as a possible contributive factor in axonal pathology, will also be examined. The experiments relate to the problem of defining the extent to which functional loss in traumatic paraplegia and paraparesis is be due to factors other than direct destruction of axons, particularly their demyelination and incomplete remyelination. This will address the utility of attempting to develop therapy for these currently untreatable conditions through improvement of remyelination or treatment of demyelination pathophysiology. The study will provide information on the role of the myelin sheath in action potential conduction, and the physiological effects of demyelination and remyelination in the central nervous systems. This basic knowledge will also be of significance outside the particular context of spinal trauma.
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