Rice D C
Toxicology Research Division, Health Canada, Ottawa, Ontario, Canada.
Neurotoxicol Teratol. 1998 May-Jun;20(3):275-83. doi: 10.1016/s0892-0362(97)00099-8.
Although it is established that developmental methylmercury exposure produces severe motor and sensory impairment, the effect on cognitive function is less clear. To explore this issue, monkeys with robust methylmercury-induced deficits in visual, auditory, and somatosensory function were tested on a series of tasks assessing central processing speed, which is highly correlated with intelligence in humans. Five monkeys (Macaca fascicularis) were dosed from birth to 7 years of age with 50 micrograms/kg/day of mercury as methylmercuric chloride. Blood mercury levels were stable at 0.8-1.1 micrograms/g until cessation of dosing. When they were 20 years old, these monkeys and four age- and rearing-matched controls were tested on a series of simple and complex reaction time tasks. The monkey sat in a primate chair with a stainless steel bar centered at waist height. Four push buttons equidistant from the steel bar were mounted on a vertical Plexiglas panel in front of the monkey. The monkey was required to make contact with the bar, then release the bar and push the appropriate button in response to a change in stimulus conditions. For the first task (simple reaction time), the monkey was required to respond on a button when it changed from unlit to red. The monkey then performed a sequence of complex reaction time tasks: two-button, four-button, and several tasks of increasing complexity using four buttons and multiple colors. For each task, the latency to release the bar after the stimulus change (central processing speed) and to move the hand from the bar to the button (motor speed) were determined. Lastly, the monkey was required to make the quickest possible motor response on the simple reaction time task. There were no differences between groups on any aspect of the experiment. These data provide further evidence for absence of cognitive impairment in monkeys exposed developmentally to methylmercury.
虽然已经确定发育期接触甲基汞会导致严重的运动和感觉障碍，但对认知功能的影响尚不清楚。为了探究这个问题，对视觉、听觉和躯体感觉功能因甲基汞而出现严重缺陷的猴子进行了一系列评估中枢处理速度的任务测试，中枢处理速度与人类智力高度相关。五只猕猴（食蟹猴）从出生到7岁每天被喂食50微克/千克的氯化甲基汞形式的汞。在停止给药前，血汞水平稳定在0.8 - 1.1微克/克。当它们20岁时，对这些猴子和四只年龄及饲养条件匹配的对照猴子进行了一系列简单和复杂反应时间任务的测试。猴子坐在灵长类动物椅上，不锈钢杆位于腰部高度的中心位置。在猴子前方的垂直有机玻璃面板上安装了四个与不锈钢杆等距的按钮。猴子需要接触杆，然后松开杆并根据刺激条件的变化按下相应按钮。对于第一个任务（简单反应时间），当灯从不亮变为红色时，猴子需要按下一个按钮做出反应。然后猴子进行了一系列复杂反应时间任务：两按钮、四按钮以及使用四个按钮和多种颜色的几个复杂度递增的任务。对于每个任务，测定刺激变化后松开杆的潜伏期（中枢处理速度）以及将手从杆移到按钮的潜伏期（运动速度）。最后，要求猴子在简单反应时间任务中做出尽可能快的运动反应。在实验的任何方面，两组之间均无差异。这些数据为发育期接触甲基汞的猴子不存在认知障碍提供了进一步的证据。
