Anoxic Injury of Central Myelinated Axons: Nonsynaptic Ionic Mechanisms
The pathophysiology of stroke and central nervous system (CNS) trauma can now be effectively studied at a molecular level. This research is concerned with understanding how cells in the brain, devoid of oxygen and/or metabolic substrates, are injured and ultimately destroyed. The reasonable presumption is that knowledge about the fundamental mechanisms of cell injury will yield clinically applicable insights relevant to how the brain may be protected during periods of disrupted perfusion or metabolism. This work can be subdivided into the study of how each of the major cellular compartments in the brain, i.e., neuronal cell bodies and dendrites, axons and glial cells, are injured by anoxia/ischemia. While great progress has been made in analyzing the mechanisms of neuronal injury in gray matter (GM) areas such as cortex, much less is known about how anoxia/ischemia damages glial cells and axons. We have been interested in the pathophysiology of CNS axonal injury and have developed a reliable model system for studying the basic mechanisms of injury to CNS-myelinated axons caused by anoxia (Stys et al. 1990a; Ransom et al. 1993). The nonsynaptic ionic mechanisms which are critical in the development of irreversible anoxic injury in white matter (WM) are the focus of this review.
KeywordsIschemia Lipase Shrinkage Retina Neurol
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