Extrapyramidal signs such as tremor, chorea or athetosis1, 2) indicating the possible involvement of dopaminergic impairment by MM in the nigrostriatal system are often detectable in cases of methylmercury (MM) intoxication. Various biochemical changes of enzymes relevant to neurotransmitters in the brain have been reported in the toxic phase of MM exposure in vivo3, 4). However, they seem to appear only after other symptoms have become detectable. In vitro treatment of methylmercury chloride (MMC) impaired the activity of tyrosine hydroxylase and DOPA decarboxylase5), the high affinity uptake of dopamine (DA)6) and the binding of D2 dopaminergic receptors7, 8). However, the concentrations necessary to produce significant inhibition were considerably higher than those seen in cases of MM intoxication. The acute response of the central dopaminergic nervous system to MM is poorly understood, because even the clinical symptoms, if any, of small doses and short term exposure to MM are unknown. On the other hand, it is known that DA release is evoked by electrical stimulation from dopaminergic terminals and that the released DA is quickly taken up into the terminals9, 10). To elucidate the sensitivity of the release mechanism of DA to acute MM exposure, we examined the effects of MMC and mercury chloride (II) (HgCl2) on the evoked release and uptake of 3H-DA in guinea pig striatal slices.