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The tumor necrosis factor (TNF) superfamily includes representative cytokines that participate in the inflammatory response as well as cell survival, and apoptosis. In this study, we found that administration of methylmercury selectively induced TNF-\u03b1 expression in the brain of mice. Although the accumulated mercury concentration in the liver and kidneys was greater than in the brain, TNF-\u03b1 expression was induced to a greater extent in brain. Thus, it is possible that there may exist a selective mechanism by which methylmercury induces TNF-\u03b1 expression in the brain. We also found that TNF-\u03b1 expression was induced by methylmercury in C17.2 cells (mouse neural stem cells) and NF-\u03baB may participate as a transcription factor in that induction. Further, we showed that the addition of TNF-\u03b1 antagonist (WP9QY) reduced the toxicity of methylmercury to C17.2 cells. In contrast, the addition of recombinant TNF-\u03b1 to the culture medium decreased the cell viability. We suggest that TNF-\u03b1 may play a part in the selective damage of the CNS by methylmercury. 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