Status epilepticus induces delayed neuronal death whose origins are not clearly defined. Because status epilepticus significantly enhances astrocytic Ca2+ signaling in vivo (See Ding S. et al., SFN abstract 2005), which in turn evokes the release of glutamate, we asked whether pharmacological treatments that impair gliotransmission impact neuronal death. Using Fluoro-Jade B (FJB), a fluorescent marker that specifically stains degenerating neurons, we found that a 1 hr period of pilocarpine-induced status epilepticus caused widespread FJB staining which was otherwise absent in control mice. Since the peak of delayed neuronal death was temporally coincident with enhanced astrocytic Ca2+ signaling we asked whether gliotransmission could contribute to this delayed neuronal death. Administration of the mGluR antagonist MPEP for 3 days reduced astrocytic Ca2+ oscillations and significantly reduced the number of FJB-labeled cells in both the cortex (P<0.05) and hippocampus (P<0.05). Glutamate released from astroc...