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REVIEW : Physical Injury of Neurons: Important Roles for Sodium and Chloride Ions

Department of Physiology The Ohio State University Columbus, Ohio

Dennis G. Emery

Department of Zoology and Genetics lowa State University Ames, Iowa

Lisa J. Rosenberg

Department of Physiology The Ohio State University Columbus, Ohio

There is growing evidence that ions other than Ca²+ play important roles in the deterioration of neuronal elements in both gray and white matter after physical injury. This review features information gathered with a tissue culture model of dendrite transection regarding the contributions of Na+ and CI^- to ultrastructural damage and neuronal death. This information and the results of other in vitro investigations of physical and ischemic/excitotoxic injuries indicate that elevation of internal Na+ is an early event that may contribute significantly to neuronal injury through effects on Na⁺-driven transport mechanisms. Proposed deleterious consequences include cytoplasmic acidification, reduced mitochondrial energy production, and elevation of intracellular Ca²⁺ and extracellular excitatory amino acids to toxic levels. Prevention of Na⁺ entry into neurons after injury has been found to limit ultrastructural damage, prevent death, and preserve electrophysiological function. Although the role of CI^- in neuronal injury is less well defined, there is also evidence that elevation of intracellular CI^- contributes to structural damage, particularly to the smooth endoplasmic reticulum. In terventions that limit Na+- and CI^--mediated damage to injured neurons may have utility in neurosurgery and as acute phase treatments for nervous system trauma and other pathological states. NEURO SCIENTIST 3:89-101, 1997

Key Words: KEY WORDS Nervous system trauma • Axotomy • Neuronal death • Calcium • Ultrastructure

The Neuroscientist, Vol. 3, No. 2, 89-101 (1997)
DOI: 10.1177/107385849700300208


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