It is now recognized that neural death associated with acute insults such as trauma, hypoglycemia, seizures, global hypoxia, and stroke is due in part to calcium-mediated excitotoxic injury (for review see ref. [1]). More specifically, acute insult stimulates excessive release of excitatory amino acid neurotransmitters (EAAs) that in turn cause a rapid influx of calcium ions in affected neurons (2). Intracellular calcium is essential for normal neural function; however, calcium overload may disrupt cell metabolism, cell excitability, gene expression, and other vital functions (3). Although the process by which calcium-mediated excitotoxic injury occurs may vary (4), the end result of compromised cell function inevitably contributes to cell death.
