【作者】 李秀芳； 马建元； 胡徽东； 阮迪云；

【机构】 解放军105医院； 中国科技大学；

【摘要】 目的慢性铅暴露可以引起儿童学习记忆和认知功能的损伤。突触可塑性被认为是学习记忆的神经生物学基础,长时程增强(long-term potentiation LTP)是突触可塑性的一种重要形式。已有的研究表明慢性铅暴露损伤了大鼠海马CA1区和齿状回LTP的诱导和表达过程。本文应用离体脑片电生理技术研究了复方多康宁(Co-DKL)对慢性铅暴露引起的发育中大鼠海马突触可塑性损伤的修复效应;方法新生Wistar幼鼠出生后经母乳摄入铅和在铅暴露的同时往食物中添加三种不同剂量的Co-DKL(0．8、1．6、3．2mg／kg／day)。在30～ 32天的大鼠海马CA1区记录EPSP;结果慢性铅暴露损伤了CA1区LTP的损伤,而高剂量Co-DKL的修复作用较小且稍有一点毒副作用。合适剂量的Co—DKL能有效逆转铅造成的神经系统损伤,可能具有一定的促智作用;结论低剂量的Co—DKL(正常剂量的二倍)对铅引起的损伤有显著的修复作用,对对照组大鼠有一定的促智作用,且没有副作用,中剂量(正常剂量的四倍)有一定的修复作用,但高剂量的修复作用较小,有一定的毒副作用。更多还原

【Abstract】 Lead (Pb) may cause a variety of learning, memory and cognitive dysfunction for children. Long-term potentiation (LTP), an important form of synaptic plasticity, is believed to underlie learning and memory. Previous studies have demonstrated that Pb impairs LTP of CAI and Dentate gyrus(DG) regions in developing rat hippocampus. This paper investigated whether pb-induced impairment of synaptic plasticity could be reversed by the Co-DKL. Neonatal wistar rats were exposed to pb from parturition by drinking of 0.2% AcPb solution or a diet supplemented with three different dosages Co-DKL(0.8、1.6、3.2mg/kg/day) with 0.2%AcPb. Excitatory postsynaptic potentials(EPSPs)were recorded in the hippocampal CAI region of rats(30-32days). The results showed that Pb reduced the amplitude of LTP significantly. In pb-exposed rats, three dosages of Co-DKL had a different effect on the amplitudes of rat hippocampal LTP. Low dosage Co-DKL almost restored the Pb-induced impairments and might have an effective role for improving intelligence, while effective role of the middle and high dosages Co-DKL was less than low dosage, and high dosage Co-DKL had a little toxicity.更多还原