Neuronal apoptosis after CNS injury: the roles of glutamate and calcium.
While a role has been well established for excitotoxic necrosis in the pathogenesis of traumatic or ischemic damage to the CNS, accumulating evidence now suggests that apoptosis may also be a prominent contributor. In this review we focus on the role of glutamate and attendant intracellular calcium influx in triggering or modifying excitotoxic necrosis and apoptosis, raising the possibility that calcium influx may affect these two death pathways in opposite directions. Incorporating consideration of both pathways will probably be needed to develop the most effective neuroprotective treatments for CNS injury.
Zipfel
G J
GJ
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri 63110, USA.
Babcock
D J
DJ
Lee
J M
JM
Choi
D W
DW
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism*; D006801:Humans; D009336:Necrosis; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D009498:Neurotoxins / Q000378:metabolism
D018696:Neuroprotective Agents; D009498:Neurotoxins; D018698:Glutamic Acid; D002118:Calcium