Reed Miranda N, Paletz Elliott M, Newland M Christopher
Experimental Psychology, Auburn University, Thach Hall, Auburn, AL 36830, USA.
Neurotoxicology. 2006 Sep;27(5):721-32. doi: 10.1016/j.neuro.2006.03.022. Epub 2006 Apr 15.
Selenium, a nutrient, and methylmercury, a developmental neurotoxicant, are both found in fish. There are reports that selenium sometimes ameliorates methylmercury's neurotoxicity, but little is known about the durability of this protection after low-level gestational exposure. Developmental methylmercury exposure disrupts behavioral plasticity, and these effects extend well into adulthood and aging. The present experiment was designed to examine interactions between developmental low-level methylmercury and nutritionally relevant dietary selenium on discrimination reversals in adulthood. Female rats were exposed, in utero, to 0, 0.5, or 5 ppm mercury as methylmercury via drinking water, approximating mercury exposures of 0, 40, and 400 microg/kg/day. They also received both prenatal and postnatal exposure to a diet containing selenium from casein only (0.06 ppm) or 0.6 ppm selenium, creating a 2 (chronic Se)x3 (gestational MeHg) full factorial design, with six to eight rats per cell. Behavior was evaluated with a spatial discrimination procedure using two levers and sucrose reinforcers. All groups acquired the original discrimination similarly. Rats exposed to low selenium (0.06 ppm), regardless of MeHg exposure, required more sessions to complete the first reversal and made more omissions during this reversal than high selenium (0.6 ppm) animals, but the two diet groups did not differ on subsequent reversals. Rats exposed to MeHg, regardless of selenium exposure, made more errors than controls on the first and third reversals, which was away from the original discrimination. MeHg-exposed animals also had shorter choice latencies than controls during the first session of a reversal. Low selenium increased the number of omissions during a reversal, whereas high MeHg exposure produced perseverative responding (errors) on the lever that was reinforced during the original discrimination. However, there was no interaction between selenium and MeHg exposure.
鱼类中同时含有营养物质硒和发育神经毒物甲基汞。有报告称,硒有时可减轻甲基汞的神经毒性,但对于孕期低水平接触后这种保护作用的持续性却知之甚少。发育过程中接触甲基汞会破坏行为可塑性,且这些影响会一直持续到成年期和老年期。本实验旨在研究发育过程中低水平甲基汞与营养相关的膳食硒之间的相互作用对成年期辨别逆转的影响。雌性大鼠在子宫内通过饮用水接触0、0.5或5 ppm的甲基汞汞,分别相当于0、40和400微克/千克/天的汞暴露量。它们在产前和产后还分别接触仅含酪蛋白硒(0.06 ppm)或0.6 ppm硒的饮食,形成2(慢性硒)×3(孕期甲基汞)的全因子设计,每个单元格中有六至八只大鼠。使用两个杠杆和蔗糖强化剂通过空间辨别程序评估行为。所有组获得初始辨别的情况相似。无论甲基汞暴露情况如何,接触低硒(0.06 ppm)的大鼠比高硒(0.6 ppm)动物完成第一次逆转需要更多的实验次数,并且在此逆转过程中出现更多遗漏,但两个饮食组在后续逆转中没有差异。无论硒暴露情况如何,接触甲基汞的大鼠在第一次和第三次逆转时比对照组犯更多错误,这些错误与初始辨别相反。接触甲基汞的动物在逆转的第一阶段的选择潜伏期也比对照组短。低硒增加了逆转过程中的遗漏次数,而高甲基汞暴露则在初始辨别时得到强化的杠杆上产生持续反应(错误)。然而,硒和甲基汞暴露之间没有相互作用。