Environmental and Occupational Health Sciences Institute, a joint Institute of the Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey and Rutgers, the State University of New Jersey, Piscataway, NJ 08854, United States.
Neurotoxicology. 2011 Jan;32(1):83-99. doi: 10.1016/j.neuro.2010.09.004. Epub 2010 Sep 25.
Lead (Pb) and stress co-occur as risk factors, share biological substrates and produce common adverse effects. We previously found that prenatal restraint stress (PS) or offspring stress (OS) could enhance maternal Pb-induced behavioral, brain neurotransmitter level and HPA axis changes. The current study examined how lifetime Pb exposure, consistent with human environmental exposure, interacts with stress. Dams were exposed to Pb beginning 2 mos prior to breeding (0, 50 or 150ppm in drinking water), PS on gestational days 16 and 17, or the combination. Offspring continued on the same Pb exposure as the dam. A subset of Pb+PS offspring also received 3 additional stress challenges (OS), yielding 9 exposure groups/gender: 0-NS, 0-PS, 0-OS, 50-NS, 50-PS, 50-OS, 150-NS, 150-PS and 150-OS. As with maternal Pb (Virgolini et al., 2008a), lifetime Pb and stress influenced Fixed Interval (FI) behavior primarily in females. Relative to 0-NS control, reductions in postreinforcement pause (PRP) times were seen only with combined Pb+PS (50-PS, 50-OS, 150-PS). Stress increased FI response rates when Pb alone was without effect (150-PS, 150-OS), but gradually mitigated rate increases produced by Pb alone (50-PS, 50-OS), effects that appear to be due primarily to PS, as they were of comparable magnitude in PS and OS groups. Individual subject data suggest that enhanced Pb and PS effects reflect increasing numbers of subjects shifting to the high end of the normal range of FI performance values, consistent with a dose-response type of Pb+stress additivity. Consistent with reports of cortico-striatal mediation of both interval timing (PRP) and FI rates, principal component analyses suggested potential mediation via altered frontal cortex norepinephrine, reduced nucleus accumbens dopaminergic control and enhanced striatal monoamine control. Altered FI performance, whether occurring through changes in response rate, PRP, or both, represent behavioral inefficiency and potentially sub-optimal or even dysfunctional resource/energy use.
铅(Pb)和压力是共同存在的风险因素,它们具有共同的生物学基础,并产生共同的不良影响。我们之前发现,产前束缚应激(PS)或后代应激(OS)可以增强母体 Pb 引起的行为、大脑神经递质水平和 HPA 轴变化。本研究探讨了终生 Pb 暴露如何与压力相互作用,这与人类的环境暴露一致。在配种前 2 个月,母鼠开始暴露于 Pb(饮用水中 0、50 或 150ppm),在妊娠第 16 和 17 天接受 PS,或两者结合。后代继续接受与母鼠相同的 Pb 暴露。一部分 Pb+PS 后代还接受了 3 次额外的应激挑战(OS),共产生了 9 个暴露组/性别:0-NS、0-PS、0-OS、50-NS、50-PS、50-OS、150-NS、150-PS 和 150-OS。与母体 Pb 一样(Virgolini 等人,2008a),终生 Pb 和应激主要影响雌性的固定间隔(FI)行为。与 0-NS 对照组相比,仅在 Pb+PS 联合处理组(50-PS、50-OS、150-PS)中观察到强化后停顿(PRP)时间减少。当单独使用 Pb 时,应激会增加 FI 反应率(150-PS、150-OS),但逐渐减轻单独使用 Pb 引起的反应率增加(50-PS、50-OS),这些影响似乎主要是由 PS 引起的,因为它们在 PS 和 OS 组中的作用相当。个体受试者数据表明,增强的 Pb 和 PS 效应反映了越来越多的受试者向 FI 性能值正常范围的高端转移,这与 Pb+应激的剂量-反应类型相加一致。与皮质纹状体对间隔计时(PRP)和 FI 率的调节一致,主成分分析表明,通过改变前额叶皮层去甲肾上腺素、减少伏隔核多巴胺能控制和增强纹状体单胺能控制来进行潜在的调节。FI 性能的改变,无论是通过反应率、PRP 还是两者的改变,都代表行为效率低下,可能是资源/能量利用不理想甚至功能失调。