Adolescent methylmercury exposure: Behavioral mechanisms and effects of sodium butyrate in mice.
Adolescent methylmercury exposure: Behavioral mechanisms and effects of sodium butyrate in mice.
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DOI：
10.1016/j.neuro.2018.10.011
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发表时间：
2019-01
期刊：
影响因子：
3.4
通讯作者：
Newland MC
中科院分区：
文献类型：
--
作者：
Boomhower SR;Newland MC
甲基汞（MeHg）是一种主要存在于鱼类体内的环境神经毒物，在妊娠期接触甲基汞会产生神经行为障碍。其他发育时期，如青春期，是否对甲基汞暴露的行为影响表现出更大的脆弱性，这只是刚刚开始探索。此外，对于反复使用赖氨酸去乙酰化酶抑制剂（如丁酸钠（NaB））对操作行为的影响知之甚少。在实验1中，雄性C57BL6/n小鼠从出生后第21天至第60天（小鼠青春期）通过饮用水暴露于0、0.3和3.0 ppm的甲基汞（n = 12）。成年后，小鼠在一系列固定比例的牛奶强化计划下接受杠杆按压训练，这些计划是为了利用强化数学原理提供的框架来分析操作行为的三个重要参数。青少年甲基汞暴露剂量依赖性地增加了饱和率，这是一种强化物追溯作用范围的测量，并且相对于对照组减少了最小反应时间。在实验2中，研究了单独使用NaB和青少年MeHg暴露后反复使用NaB的行为影响。雄性C57BL6/n小鼠在青春期给予0或3.0 ppm的甲基汞，在行为测试之前，两周内每天一次滴注生理盐水或0.6 g/kg NaB（每个细胞n = 12）。青少年接触甲基汞再次增加饱和率，但没有显著改变最小反应时间。NaB也增加了MeHg暴露组的饱和率。这些数据表明，青少年甲基汞暴露和NaB的行为机制可能与强化对先前反应的影响有关。具体来说，MeHg和NaB将强化物的作用集中在最近的反应上。
Methylmercury (MeHg), an environmental neurotoxicant primarily found in fish, produces neurobehavioral impairment when exposure occurs during gestation. Whether other developmental periods, such as adolescence, display enhanced vulnerability to the behavioral effects of MeHg exposure is only beginning to be explored. Further, little is known about the effects of repeated administration of lysine deacetylase inhibitors, such as sodium butyrate (NaB), on operant behavior. In Experiment 1, male C57BL6/n mice were exposed to 0, 0.3, and 3.0 ppm MeHg (n = 12 each) via drinking water from postnatal days 21 to 60 (murine adolescence). As adults, mice were trained to lever press under an ascending series of fixed-ratio schedules of milk reinforcement selected to enable the analysis of three important parameters of operant behavior using the framework provided by Mathematical Principles of Reinforcement. Adolescent MeHg exposure dose-dependently increased saturation rate, a measure of the retroactive reach of a reinforcer, and decreased minimum response time relative to controls. In Experiment 2, the behavioral effects of repeated NaB administration both alone and following adolescent MeHg exposure were examined. Male C57BL6/n mice were given either 0 or 3.0 ppm MeHg during adolescence and, before behavioral testing, two weeks of once daily i.p. injections of saline or 0.6 g/kg NaB (n = 12 in each cell). Adolescent MeHg exposure again increased saturation rate but did not significantly alter minimum response time. NaB also increased saturation rate in both MeHg exposure groups. These data suggest that the behavioral mechanisms of adolescent MeHg exposure and NaB may be related to the impact of reinforcement on prior responses. Specifically, MeHg and NaB concentrated the effects of reinforcers onto the most recent responses.
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