Role of Excitatory Amino Acids in Neuronal and Glial Responses to Traumatic Brain Injury

Following traumatic brain injury (TBI), many neuronal cells are metabolically deranged at the subcellular level, but are not primarily disrupted. Several studies employing experimental models have indicated that neuronal cells subjected to TBI are more vulnerable to a secondary ischemic insult (e.g., Jenkins et al., 1989), implying that these cells are dysfunctional metabolically. One major goal of therapies for TBI during the acute period is to provide an ideal milieu for the recovery of these cells. To establish appropriate therapies for TBI, it is crucial to delineate the sequence of cellular and subcellular events that lead traumatized neuronal cells to undergo metabolic derangements. This chapter discusses the events that naturally begin from the moment of injury.