Electrogenesis of sustained potentials
The weight of evidence, as of this date, is in favor of the hypothesis of a predominantly glial generation of the SP shifts which are evoked by repetitive stimulation of afferent nerves or of fiber tracts. Unlike electrically evoked SP shifts, the SP shifts associated with spreading depression are probably generated by massive depolarization of all cells, glia as well as neurones. For SP shifts related to more physiological process, such as the contingent negative variation, the SP shifts or positive reinforcement and the related 'consummatory potential', the evidence is insufficient even for a tentative conclusion. SP shifts of varying intensity are associated with a proportional increase of oxidative energy turnover. During spreading depression the electron transport of the oxidative enzyme chain is accelerated well beyond the level observed in healthy cortex. The cause of spreading depression is not a shortage of the supply of oxidative energy. Dorsal root potentials do not significantly contribute to SP shifts of the spinal cord, nor do SP shifts appear to cause dorsal root potentials. There is no convincing reason at this time to suggest that under normal conditions neurones are influenced by sustained currents flowing in the extracellular medium. The more intense extracellular currents occurring during pathological conditions may possibly contribute to spreading depression and/or other types of paroxysmal activity. More quantitative data are badly needed to decide these fundamental questions. The curious immunity of the spinal cord and of the immature brain to spreading depression challenges the ingenuity of the pathophysiologist. © 1973.
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