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作 者:张亨山[1] 赵西龙[1] 宋丽华[1] 秦钰慧[1]
出 处:《中华预防医学杂志》1997年第5期285-287,共3页Chinese Journal of Preventive Medicine
摘 要:为了探讨铅损害学习记忆功能的神经生物学机制,采用大鼠海马脑片观察铅在体外对谷氨酸递质释放的影响。结果显示,3.1~50.0μmol/L铅使海马脑片无钙状态下的3H-DL-谷氨酸自发性释放量增加23.2%~66.2%,并有剂量-效应关系。但在含钙介质中,当铅染毒剂量从1.0μmol/L增加为50.0μmol/L时,3H-DL-谷氨酸的自发性释放量减少22.6%~55.3%,而高钾去极化释放量增加89.3%~332.1%,而且均存在剂量-效应关系。表明铅对谷氨酸递质自发性和去极化释放过程均有干扰作用。Effects of lead on the release of glutamate neurotransmitter were observed in rat hippocampal slices in vitro to study its neurobiological mechanism of lead induced impairment in learning and memory function. Results showed that exposure to 3.1 to 50.0 μmol/L of lead could cause a dose dependent increase in spontaneous release of 3H DL glutamic acid in hippocampal slices by 23.2% to 66 2% in the absence of calcium. However, in the presence of calcium, spontaneous release of 3H DL glutamic acid decreased by 22.6% to 55.3% with increase of exposure to lead from 1.0 to 50.0 μmol/L, and the release induced by potassium increased by 89.3% to 332.1% with a dose response relationship. It indicated that exposure to lead could interfere with spontaneous and induced release of glutamate transmitter.
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