Perinatal exposure to low doses of methylmercury (MeHg) can cause neurological symptoms in adults. Instead of causing net cell loss, it is assumed that toxic substances differentiate and neurological functions change, such as catecholamine can be transmitted. We use embryonic stem cells to differentiate neural inbreeding (system) to explore this subtle toxicity. Cultures of mixed nerves formed TH-positive tyrosine dopaminergic neurons and specific functions, such as dopamine transport activity, within 20 days. The difference of these six days is that the mature nerves are buried in advance. During this period, exposure to methylmercury down-regulated the transcripts of several neurons, but did not affect the genes of cells, or caused measurable household losses. The neurotransmitter system of mRNAs spectrum shows that there are few down-regulated dopamine receptors, but it is known that anti-regulation systems, such as galanin receptor 2, are regulated. The short incubation period of chronic (6 days) but not exposed to methylmercury weakened the expression level of endogenous neurotrophic factors needed by mature cells. Therefore, the cell size, the most beautiful population reduction activity lost its signature function. When mixed lineages are blocked by kinase activity exposed to methylmercury, the most beautiful activity and repair are avoided. Therefore, the influence of transcription pattern on the recognition of pathogenic methylmercury neurons proves that drug intervention is specifically to protect these cells.