Abstract

Nursery-reared rhesus monkeys were treated with no or moderate levels of lead during the first year postpartum. Previously, the lead-treated monkeys exhibited behaviors in the nonhuman primate version of the open field (10) resembling those caused by hippocampal lesions. The current study investigated the mechanism(s) underlying these lead-related effects using a cholinergic agonist (arecoline) and antagonist (scopolamine) as pharmacological probes that were administered prior to open field testing at 5 and 6 years of age, respectively. Arecoline decreased locomotion and number of sectors entered. Scopolamine decreased defecation frequency. Neither drug interacted with prior lead treatment, indicating limited cholinergic involvement in the expression of these alterations. The lead-treated subjects continued to exhibit alterations as previously reported (10); specifically, a longer latency to enter the open field, increased frequency and duration of environmental exploration and, at 5 years of age, decreased duration of inactivity in the open field. These effects were seen four and five years after lead treatment ended and nearly three and four years after blood lead levels had declined to ≤5 μg/dL. Although latency to enter and duration of inactivity seem to be approaching control levels, the increased exploration does not.

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