Methylmercury chloride was administered PO to male Kud: ddY mice at a dose of 5 mg/kg/day for 20 days. The contents of taurine, aspartate, glutamate, glycine, and gamma-aminobutyric acid were determined in tissue and crude synaptosomal (P2) fraction of cerebellum, cerebral cortex, and spinal cord of methylmercury-treated mice with or without ataxia. In the cerebellum of ataxic mice, increased levels of taurine and glycine were found in the tissue and P2 fraction, and increased levels of glutamate were found in the P2 fraction. In the cerebral cortex, the levels of gamma-aminobutylic acid decreased in the tissue and in the P2 fraction of ataxic mice, but increased levels were found in the tissue of non-ataxic mice. A decreased aspartate level in the cerebral cortex of ataxic mice and an increased taurine level in the cerebral cortex of non-ataxic mice were also found. In the spinal cord of ataxic mice, taurine increased in the tissue and in the P2 fraction. Glutamate level decreased in the spinal cord of ataxic mice, but increased in the P2 fraction of non-ataxic mice. Increased glycine levels in the P2 fraction of the spinal cord were also found in non-ataxic mice. Histologically, some degenerative changes were demonstrated in the cerebral and cerebellar cortices of ataxic mice. Such changes were also present to a mild degree in non-ataxic mice. In conclusion, methylmercury treatment altered the levels of putative neurotransmitter amino acids in neural tissue of mice. These alterations might be caused by specific neural cell dysfunction and could be related to the appearance of ataxia.