Yuri Ikeda-Matsuo

TL;DR: The induction of microsomal PGE synthase 1 (mPGES-1) is demonstrated, an inducible terminal enzyme for PGE(2) synthesis, in neurons, microglia, and endothelial cells in the cerebral cortex after transient focal ischemia in mice, suggesting that mPGes-1 may be a critical determinant of postischemic neurological dysfunctions and a valuable therapeutic target for treatment of human stroke.

TL;DR: It is shown that astrocytes play an essential role in the induction of brain ischemic tolerance, and that upregulation of P2X7 receptors in astroCytes is essential, and the results suggest that hypoxia-inducible factor-1α, a well known mediator of ischeic tolerance, is involved in P2x7 receptor-mediated ischeMIC tolerance.

TL;DR: The results suggest that the activation of microglia contributes to PGE2 production through the concerted de novo synthesis of mPGES‐1 and COX‐2 at sites of inflammation of the brain parenchyma.

TL;DR: Dysregulation in GABAA depolarizing activity delayed dendritic development and reduced NPC proliferation resulting in decreased neuronal density.

TL;DR: It is demonstrated here that MARCKS was translocated from cytosol to detergent‐resistant membrane microdomains, known as lipid rafts, within 30 min after insulin‐like growth factor‐I (IGF‐I) stimulation, which was accompanied by MARC KS dephosphorylation, β‐actin accumulation in lipid rafting, and lamellipodia formation.