Neutrophil infiltration into brain parenchyma is transiently observed during the acute phase of SE (4 - 36 hr after SE) and disappears thereafter [20]. SE rapidly increases synthesis and release of chemokines in various areas of the rodent brain [42]. Among them, MIP-2 is required for efficient neutrophil or lymphocyte recruitment to brain parenchyma [43]. In our previous study [20], neutrophil infiltration in the frontoparietal cortex was regulated by P2X7 receptor-mediated MIP-2 expression. In the PC, however, neither a P2X7 receptor agonist/antagonist nor IL-1Ra (an IL-1β antagonist) infusion could not affect leukocyte infiltration. In the present study, sTNFp55R infusion effectively inhibited neutrophil infiltration in the PC by reducing vasogenic edema formation in a MIP-2-independent manner. With respect to the present and our previous reports, it is therefore likely that vasogenic edema induced by TNF-α can induce neutrophil infiltration and press injury to evoke neuronal-astroglial loss in the PC, unlike other brain regions.