lls in various pathophysiological conditions, including SE [17,18]. TNF-α shows various effects on brain function depending on its local tissue concentration, the type of target cells, and especially the specific receptor subtype: TNF receptor I, or p55 receptor (TNFp55R); and TNF receptor II, or p75 receptor (TNFp75R) [19]. Furthermore, TNF-α induces macrophage inflammatory protein-2 (MIP-2) that recruits neutrophils under pathological conditions, including SE [14,20]. Neurons, microglia, and astrocytes produce MIP-2 when incubated with pro-inflammatory cytokines such as TNF-α and/or interleukin-1β (IL-1β) or after injury [21-23]. Indeed, we have recently reported that SE-mediated MIP-2 expression is relevant to leukocyte