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