Activation of PI3K/Akt mediates neuroprotection. (a) Neuroprotection by dexamethasone is mediated by GR and PI3K. Cerebral infarct volume after MCAo in response to dexamethasone (20 mg/kg), RU486 (200 mg/kg) and LY294002 (5 mg/kg, n = 7–11). Vehicle and dexamethasone groups are identical to those in figure 1a. *P < 0.05 vs. vehicle, **P < 0.05 vs. dexamethasone. RU, RU486; LY, LY294002. (b) In vivo activation of PI3K by dexamethasone. PI3K activity from mouse brain tissue immunoprecipitated with GR or p85 antibody. The product of the kinase reaction, PIP3, was visualized by autoradiography. (c) The left panel shows Akt activity and total Akt from mouse brain tissue. Mice were treated with vehicle or dexamethasone, with or without actinomycin D (ActD) (5 mg/kg), RU486, or LY294002. The right panel shows P-Akt (S473) and total Akt from mouse aortae. P, phosphorylation form of the protein. Representative experiments are shown.