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Astrocyte activation plays an important role in neuronal damage induced by ischemia. In the present study, we confirmed that the presence of both the N-methyl-D-aspartate (NMDA) subtype and α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptors in astrocytes is critical for the induction of glial cell proliferation in an in vitro model of ischemia-reperfusion. To investigate the cellular and molecular mechanisms by which astrocytes promote neuronal damage in an in vivo ischemic model, we examined the effects of the astrocyte-specific NMDA receptor antagonist, MK-801, on glial cell proliferation and neuronal damage in gerbils following middle cerebral artery occlusion (MCAO). After either partial or complete ischemia, MK-801 reduced glial cell proliferation at the lesion site. As assessed by immunohistochemistry, MK-801 reduced the number of activated microglia and enhanced the expression of the anti-
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