The consequences of developmental exposure to methylmercury on behavior in aged animals were investigated. Methylmercury exposure was arranged by placing 0, 0.5 or 6.4 ppm Hg in the drinking water of female rats at least 4 weeks before mating and continuing until postnatal (PN) day 16. Brain Hg concentrations in cohorts of low-and high-dose offspring were 0.5 and 9.1 ppm at birth and 0.04 and 0.52 ppm at weaning (described in another report). Lever pressing of female offspring was maintained under a Multiple Differential Reinforcement of High Rate 9:4 Extinction schedule of food reinforcement (Mult DRH 9:4 EXT). Under the DRH 9:4 schedule, a food reinforcer was delivered when nine responses occurred within 4 s. Under the Extinction schedule, responding had no programmed consequences. No exposure-related differences in reinforcement rate under the DRH schedule or discrimination between the DRH and extinction components were apparent initially. At 950 days of age, the overall response rates of controls had shown a gradual decline over the previous 500 days to about 80% of their beginning levels, but, otherwise, most controls were healthy. A gradual decline in the reinforcement rate began to appear in low-and high-dose rats at about 500 and 800 days of age, respectively. Microanalyses of the nine-response burst maintained by the DRH schedule revealed that the lever-press duration increased, the inter-response time (IRT) was unaffected, and the time between response bursts increased. Overall, the nine-response burst remained intact as a coherent response unit. The increased time between response bursts caused the decline in reinforcement rate. All rats displayed these effects as they aged, but the mercury-exposed rats did so sooner. D 2000 Elsevier Science Inc. All rights reserved.The hypothesis of``silent damage'' holds that neurotoxicants can act in undetectable ways until another event, such as aging, further challenges nervous system function [38,39]. Difficulties in detecting such damage could be due to the nervous system's extraordinary compensatory ability or because the threshold for neural damage has not been crossed. Delayed neurotoxicity, a necessary element of the hypothesis, is clearly established with methylmercury, especially in sensory± motor domains [4,10,32].In reports that may have prompted the original hypothesis, mice exposed during gestation to high levels of methylmercury showed progressive deterioration in swimming ability and other motor endpoints as they aged [34 ± 36]. These early reports have been supplemented by more recent studies with nonhuman primates [32]. In these, sensory ± motor function [31,32] and higher-order visual function [33] deteriorated more in aging monkeys that had been exposed during development to methylmercury than in controls.Support for the hypothesis that silent damage becomes apparent with aging is also accruing from long-term studies of individuals exposed to methylmercury. As people exposed to methylmercury during the Minamata tragedy have aged, activi...