Cadmium (Cd) is a toxic heavy metal and a significant public health concern. Epidemiological studies suggest that Cd is a potential neurotoxicant, and its exposure is associated with cognitive deficits in children, adults, and seniors. Our previous study has found that adulthood-only Cd exposure can impair cognition in mice. However, few studies have addressed the effects of Cd exposure during adolescence on cognitive behavior in animals later in life. In the present study, we exposed 4-week-old male C57BL/6 mice to 3 mg/L Cd via drinking water for 28 weeks and assessed their hippocampus-dependent learning and memory. Cd did not affect anxiety or locomotor activity in the open field test. However, Cd exposure impaired short-term spatial memory and contextual fear memory in mice. A separate cohort of 4-week-old mice was similarly exposed to Cd for 13 weeks to investigate the potential mechanism of Cd neurotoxicity on cognition. We observed that Cd-treated mice had fewer adult-born cells, adult-born neurons, and a reduced proportion of adult-born cells that differentiated into mature neurons in the subgranular zone of the dentate gyrus. These results suggest that Cd exposure from adolescence to adulthood is sufficient to cause cognitive deficits and impair key processes of hippocampal neurogenesis in mice.

中文翻译：

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青少年镉暴露损害 C57BL/6 小鼠的认知和海马神经发生

镉 (Cd) 是一种有毒的重金属，是一个重要的公共健康问题。流行病学研究表明，镉是一种潜在的神经毒物，它的暴露与儿童、成人和老年人的认知缺陷有关。我们之前的研究发现，仅成年期的 Cd 暴露会损害小鼠的认知能力。然而，很少有研究解决青春期接触镉对动物晚年认知行为的影响。在本研究中，我们通过饮用水将 4 周大的雄性 C57BL/6 小鼠暴露于 3 mg/L Cd 中 28 周，并评估它们的海马依赖性学习和记忆。在露天试验中，镉不影响焦虑或运动活动。然而，镉暴露损害了小鼠的短期空间记忆和情境恐惧记忆。一组单独的 4 周龄小鼠同样暴露于 Cd 13 周，以研究 Cd 神经毒性对认知的潜在机制。我们观察到，Cd 处理的小鼠的成体细胞、成体神经元和在齿状回颗粒下区分化为成熟神经元的成体细胞比例降低。这些结果表明，从青春期到成年期的 Cd 暴露足以导致小鼠认知缺陷并损害海马神经发生的关键过程。