PI3 kinase is required for the increase in surface AMPARs induced by TNFα. A, Pretreatment (2 h) with inhibitors for PKA (PKI, 1 μm), CaMKII (KN-93, 20 μm), COX-2 (aspirin, 10 μm), p38 MAP kinase [SB 20 3580 (SB), 50 μm], or p42-44 MAP kinase [PD 98059 (PD), 50 μm] all failed to prevent the TNFα-mediated increase in surface GluR1 (black bars; n = 40-85 per condition) relative to untreated sister cultures (gray bars). B, Group data indicating that pretreatment with wortmannin (100 nm; n = 172) or LY 294,002 (50 μm; n = 60) prevented the TNFα-induced increase in surface expression of GluR1 (black bars) compared with untreated sister cultures (gray bars). C, Sample micrographs showing the surface expression of GluR1 from sister cultures: untreated, treated with 60 nm TNFα, or pretreated with wortmannin and then treated with TNFα.