Apolipoprotein E protects against NMDA excitotoxicity.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Aono, M; Lee, Y; Grant, ER; Zivin, RA; Pearlstein, RD; Warner, DS; Bennett, ER; Laskowitz, DT

Published Date

  • October 2002

Published In

Volume / Issue

  • 11 / 1

Start / End Page

  • 214 - 220

PubMed ID

  • 12460559

International Standard Serial Number (ISSN)

  • 0969-9961

Digital Object Identifier (DOI)

  • 10.1006/nbdi.2002.0541


  • eng

Conference Location

  • United States