Newland M C, Yezhou S, Lögdberg B, Berlin M
Department of Psychology, Auburn University, Alabama 36849.
Toxicol Appl Pharmacol. 1994 May;126(1):6-15. doi: 10.1006/taap.1994.1084.
Postnatal exposure to lead or methyl mercury results in mental retardation, learning deficits, and other neurobehavioral effects in humans, and adverse consequences of prenatal exposure have been clearly documented with methyl mercury. To examine the developmental neurotoxicity of these metals, especially lead, concurrent schedules of food reinforcement were used to identify learning deficits in squirrel monkeys exposed during gestation to either methyl mercury or lead. Pregnant squirrel monkeys were administered methyl mercury (0.7 to 0.9 ppm in maternal blood) or lead (21 to 79 micrograms/dl in maternal blood) during the last half to two-thirds of gestation. At about 5-6 years of age, offspring were trained to lever press under concurrent schedules of reinforcement in which separate random interval reinforcement schedules operated independently on two levers. Reinforcement densities were varied such that 20 to 90% of the reinforcers were programmed to derive from the left lever (i.e., one lever was "richer" than the other). At steady state, the behavior of the controls was sensitive to reinforcement density and showed little lever bias, but the behavior of monkeys exposed to more than 40 micrograms/dl of lead and to methyl mercury was less sensitive to reinforcement rates and heavily biased. When relative reinforcement density on a lever changed, the unexposed animals' response rates gradually shifted to the newly rich lever. The behavior of monkeys exposed to methyl mercury or more than 40 micrograms/dl of lead changed slowly, not at all, or in the wrong direction. Steady-state behavior of monkeys exposed to less than 40 micrograms/dl resembled controls, but acquisition progressed more slowly and required 2-4 times as many reinforcers to complete. These effects suggest a behavioral mechanism--insensitivity to changing reinforcement contingencies--by which learning deficits and behavioral changes associated with these metals might be related to toxicant exposure. Since maternal blood levels corresponded to those that could be experienced in occupational settings, the present data raise the possibility of fetal hazards associated with maternal lead exposures at levels tolerated in humans in occupational settings.
出生后接触铅或甲基汞会导致人类智力发育迟缓、学习能力缺陷及其他神经行为影响，产前接触甲基汞的不良后果已有明确记录。为研究这些金属尤其是铅的发育神经毒性，采用同时进行食物强化的实验安排来确定孕期接触甲基汞或铅的松鼠猴的学习能力缺陷。怀孕的松鼠猴在孕期的后半段至三分之二期间，被给予甲基汞（母体血液中浓度为0.7至0.9 ppm）或铅（母体血液中浓度为21至79微克/分升）。在约5至6岁时，对后代进行训练，使其在同时进行的强化实验安排下按压杠杆，其中独立的随机间隔强化实验安排在两个杠杆上独立运行。强化密度有所变化，使得20%至90%的强化物被设定来自左杠杆（即一个杠杆“更丰富”）。在稳定状态下，对照组的行为对强化密度敏感，几乎没有杠杆偏向，但接触超过40微克/分升铅和甲基汞的猴子的行为对强化速率不太敏感且有严重偏向。当杠杆上的相对强化密度改变时，未接触的动物的反应速率会逐渐转向新的丰富杠杆。接触甲基汞或超过40微克/分升铅的猴子的行为变化缓慢、完全不变或方向错误。接触低于40微克/分升铅的猴子的稳定状态行为与对照组相似，但习得过程进展更慢，完成所需的强化物数量是对照组的2至4倍。这些影响表明了一种行为机制——对不断变化的强化意外情况不敏感——通过这种机制，与这些金属相关的学习能力缺陷和行为变化可能与接触毒物有关。由于母体血液水平与职业环境中可能出现的水平相当，目前的数据增加了职业环境中人类可耐受的母体铅暴露水平对胎儿产生危害的可能性。
