Abstract
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.
MeSH terms
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Animals
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Apoptosis / drug effects
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Apoptosis / physiology*
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Brain Injuries / metabolism*
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Brain Injuries / pathology
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Brain Injuries / physiopathology
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Brain Ischemia / metabolism*
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Brain Ischemia / pathology
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Brain Ischemia / physiopathology
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Calcium / metabolism*
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Calcium Signaling / physiology*
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Glutamic Acid / metabolism*
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Humans
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Necrosis
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Nerve Degeneration / metabolism*
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Nerve Degeneration / pathology
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Nerve Degeneration / physiopathology
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Neuroprotective Agents / pharmacology
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Neuroprotective Agents / therapeutic use
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Neurotoxins / metabolism
Substances
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Neuroprotective Agents
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Neurotoxins
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Glutamic Acid
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Calcium