Knockdown of AMPA receptor GluR2 expression causes delayed neurodegeneration and increases damage by sublethal ischemia in hippocampal CA1 and CA3 neurons.

ABSTRACT: Considerable evidence suggests that Ca(2+)-permeable AMPA receptors are critical mediators of the delayed, selective neuronal death associated with transient global ischemia and sustained seizures. Global ischemia suppresses mRNA and protein expression of the glutamate receptor subunit GluR2 and increases AMPA receptor-mediated Ca(2+) influx into vulnerable neurons of the hippocampal CA1 before the onset of neurodegeneration. Status epilepticus suppresses GluR2 mRNA and protein in CA3 before neurodegeneration in this region. To examine whether acute downregulation of the GluR2 subunit, even in the absence of a neurological insult, can cause neuronal cell death, we performed GluR2 "knockdown" experiments. Intracerebral injection of antisense oligodeoxynucleotides targeted to GluR2 mRNA indu

SUBMITTER: Oguro K 

PROVIDER: S-EPMC6782923 | biostudies-literature | 1999 Nov

REPOSITORIES: biostudies-literature