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In view of the known sensitivity of the developing central nervous system to pollutants, we sought to assess the effects of exposure to uranium (U) — a heavy metal naturally present in the environment — on the behavior of young rats and the impact of oxidative stress on their hippocampus. Pups drank U (in the form of uranyl nitrate) at doses of 10 or 40 mg.L-1 for 10 weeks from birth. Control rats drank mineral water. Locomotor activity in an open field and practice effects on a rotarod device decreased in rats exposed to 10 mg.L-1 (respectively, -19.4% and -51.4%) or 40 mg.L-1 (respectively, -19.3% and -55.9%) in compared with control rats. Anxiety (+37%) and depressive-like behavior (-50.8%) were altered by U exposure only at 40 mg.L-1. Lipid peroxidation (+35%) and protein carbonyl concentration (+137%) increased significantly after exposure to U at 40 mg.L-1. A significant increase in superoxide dismutase (SOD, +122.5%) and glutathione peroxidase (GPx, +13.6%) activities was also observed in the hippocampus of rats exposed to 40 mg.L-1. These results demonstrate that exposure to U since birth alters some behaviors and modifies antioxidant status. © 2015, Japanese Society of Toxicology. All rights reserved.

International audience; The central nervous system (CNS) is known to be sensitive to pollutants during its development. Uranium (U) is a heavy metal that occurs naturally in the environment as a component of the earth's crust, and populations may therefore be chronically exposed to U through drinking water and food. Previous studies have shown that the CNS is a target of U in rats exposed in adulthood. We assessed the effects of U on behavior and cholinergic system of rats exposed from birth for 10 weeks at 10 mg.L⁻¹ or 40 mg.L⁻¹. For behavioral analysis, the sleep/wake cycle (recorded by telemetry), the object recognition memory and the spatial working memory (Y-maze) were evaluated. Acetylcholine (ACh) and acetylcholinesterase (AChE) levels were evaluated in the entorhinal cortex and hippocampus. At 40 mg.L⁻¹, U exposure impaired object recognition memory (-20%), but neither spatial working memory nor the sleep/wake cycle was impaired. A significant decrease was observed in both the ACh concentration (-14%) and AChE activity (-14%) in the entorhinal cortex, but not in the hippocampus. Any significant effect on behaviour and cholinergic system was observed at 10 mg U.L⁻¹. These results demonstrate that early exposure to U during postnatal life induces a structure cerebral-dependant cholinergic response and modifies such memory process in rats. This exposure to U early in life could have potential delayed effects in adulthood.