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

Abstract

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