Exposure to lead (Pb) or polychlorinated biphenyls (PCBs) during early development has been associated with deficits in cognitive function in children (Pediatrics 87 (1991) 219; N. Engl. J. Med. 335 (1996) 783). These effects persist in the child long after exposure has ceased and body burdens have diminished. Despite intensive research, no consensus on the mechanisms of neurotoxicity of these chemicals has resulted. As the primary neurotoxic action of these agents is to impair cognitive ability, a number of laboratories have examined and reported on the detrimental the effects of Pb or PCBs on hippocampal synaptic transmission and long-term potentiation (LTP) in animals exposed during the perinatal period. Use-dependent synaptic plasticity, of which hippocampal LTP is the primary model system, is a fundamental property of neuronal function. In forebrain structures such as amygdala and hippocampus, LTP and related processes are purported to represent a physiological substrate for memory. During brain ontogeny, this type of plasticity guides the establishment and maintenance of synaptic connections in cortical structures based on sensory input. We postulate that the actions of PCBs and Pb in the developing nervous system perturb activity-dependent plasticity and promote organizational changes in brain. Aberrant connectivity derived from perturbations in activity-dependent plasticity during development may manifest as impaired LTP and cognitive ability in the adult organism.

中文翻译：

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铅或多氯联苯发育暴露的长期后果：啮齿动物中枢神经系统的突触传递和可塑性。

早期发育过程中接触铅（Pb）或多氯联苯（PCBs）与儿童认知功能缺陷有关（Pediatrics 87（1991）219; N. Engl。J. Med。335（1996）783）。在停止接触并减轻身体负担很长时间之后，这些影响仍然存在于儿童中。尽管进行了深入研究，但尚未对这些化学物质的神经毒性机制达成共识。由于这些药物的主要神经毒性作用是损害认知能力，因此许多实验室已经检查并报告了铅或多氯联苯对围产期暴露的动物海马突触传递和长期增强（LTP）的有害影响。 。使用依赖的突触可塑性，其中海马LTP是主要的模型系统，是神经元功能的基本属性。据称在杏仁核和海马体等前脑结构中，LTP和相关过程代表了记忆的生理底物。在大脑个体发育过程中，这种可塑性指导基于感觉输入的皮质结构中突触连接的建立和维持。我们假设多氯联苯和铅在发展中的神经系统中的作用扰乱了活动依赖性可塑性，并促进了大脑的组织变化。在发育过程中源自活动依赖性可塑性扰动的异常连接性可能表现为成年生物体LTP和认知能力受损。这种可塑性指导基于感觉输入的皮质结构中突触连接的建立和维持。我们假设多氯联苯和铅在发展中的神经系统中的作用扰乱了活动依赖性可塑性，并促进了大脑的组织变化。在发育过程中源自活动依赖性可塑性扰动的异常连接性可能表现为成年生物体LTP和认知能力受损。这种可塑性指导基于感觉输入的皮质结构中突触连接的建立和维持。我们假设多氯联苯和铅在发展中的神经系统中的作用扰乱了活动依赖性可塑性，并促进了大脑的组织变化。在发育过程中源自活动依赖性可塑性扰动的异常连接性可能表现为成年生物体LTP和认知能力受损。