An extensive literature indicates that the fetal brain is exquisitely sensitive to methylmercury. These data come from a multiplicity of species, including humans. Despite the extent of the current literature, however, two difficult and important questions remain unanswered. First, what are the lifetime consequences of prenatal exposure? Might they remain latent until the brain is stripped of compensatory capacity by the processes of aging? Second, what might be the consequences of lifetime exposure to relatively low levels of methylmercury? Could minute increments of damage cumulate to accelerate the processes of aging in the brain? These questions will be addressed in mice in an experimental format designed to follow the course of potential neurotoxicity through the lifespan. The mice will be exposed prenatally alone or both prenatally and postnatally. Specified groups will be observed at the age of 3, 9, 15, and 21 months for six-month periods, during which behavioral measures of motor function and cognitive performance will be secured. At the end of the observation period, brains will be examined by quantitative morphological methods to determine the structural consequences of the various exposure scenarios, and histo- chemical methods will be used for mercury localization. Both organic and inorganic content will also be assayed. These data will contribute data essential for a full risk assessment of dietary methylmercury sources, because current human data suggest adverse effects of exposure at surprisingly low levels.
