Apolipoprotein E Protects against NMDA Excitotoxicity

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