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.
Original language | English (US) |
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Pages (from-to) | 214-220 |
Number of pages | 7 |
Journal | Neurobiology of Disease |
Volume | 11 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2002 |
Keywords
- Apolipoprotein E
- Calcium influx
- Cell culture
- Cerebral ischemia
- Excitotoxicity
- Neuroprotection
- NMDA
- RAP
ASJC Scopus subject areas
- Neurology