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Apolipoprotein E Protects against NMDA Excitotoxicity

Authors
Journal
Neurobiology of Disease
0969-9961
Publisher
Elsevier
Publication Date
Volume
11
Issue
1
Identifiers
DOI: 10.1006/nbdi.2002.0541
Keywords
  • Excitotoxicity
  • Nmda
  • Apolipoprotein E
  • Cell Culture
  • Calcium Influx
  • Neuroprotection
  • Rap
  • Cerebral Ischemia
Disciplines
  • Biology

Abstract

Abstract Preclinical and clinical evidence implicates a role for endogenous apolipoprotein E in modifying the response of the brain to focal and global ischemia. To investigate whether apoE modulates the neuronal response to glutamate excitotoxicity, we exposed primary neuronal glial cultures and a neuronal cell line to biologically relevant concentrations of apolipoprotein E prior to NMDA exposure. In both of these paradigms, apolipoprotein E exerted partial protective effects. At neuroprotective concentrations, however, apolipoprotein E failed to block NMDA-induced calcium influx to the same magnitude as the NMDA receptor antagonist MK-801. These results suggest that one mechanism by which apolipoprotein E modifies the central nervous system response to ischemia may be by reducing glutamate-induced excitotoxicity.

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