While a role has been well established for excitotoxic necrosis in the path
ogenesis of traumatic or ischemic damage to the CNS, accumulating evidence
now suggests that apoptosis may also be a prominent contributor. In this re
view we focus on the role of glutamate and attendant intracellular calcium
influx in triggering or modifying excitotoxic necrosis and apoptosis, raisi
ng the possibility that calcium influx may affect these two death pathways
in opposite directions. Incorporating consideration of both pathways will p
robably be needed to develop the most effective neuroprotective treatments
for CNS injury.