论文部分内容阅读
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。
In order to investigate the neurobiological mechanism of lead-damaging learning and memory function, rat hippocampal slices were used to observe the effect of lead on glutamate neurotransmitter release in vitro. The results showed that 3.1 ~ 50.0μmol / L lead to 23.2% ~ 66.2% 3H-DL-glutamic acid spontaneous release in hippocampal slices without calcium, and there is a dose-effect relationship . However, in the calcium-containing medium, the spontaneous release of 3H-DL-glutamic acid decreased by 22.6% -55.3% when the lead exposure dose increased from 1.0μmol / L to 50.0μmol / L, While the release of high-potassium depolarization increased 89.3% ~ 332.1%, and there is dose-effect relationship. It showed that lead had an interference effect on the spontaneous and depolarization of glutamate neurotransmitter.