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，用海马突触小体和脑片分别观察了铅在体外对谷氨酸递质摄取和释放的影响。结果显示，3．1－50.0μmol／L铅使海马突触小体3H-DL-谷氨酸摄取量增加70．4％－193．2％，使脑片无钙状态下的自发性释放量增加23．2％－66．2％，并均有剂量-效应关系。但是在含钙介质中，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％，而且也均存在剂量-效应关系。提示铅不仅能促进谷氨酸递质的灭活，而且还干扰它的释放过程。这可能会影响该递质的突触传递过程及其兴奋性作用，使LTP现象减弱或不能产生。
In order to investigate the neurobiological mechanism of lead-damaging learning and memory function, the effects of lead on glutamate uptake and release in vitro were observed using hippocampal synaptosomes and brain slices. The results showed that 3.1-50.0μmol / L lead to hippocampal synaptosome 3H-DL-glutamate uptake increased by 70.4% -193.2%, so that the brain slices of calcium-free spontaneous release Increase 23.2% -66.2%, and have dose-effect relationship. However, the spontaneous release of 3H-DL-glutamic acid decreased by 22.6% -55.3% in the calcium-containing medium when the dose of lead was increased from 1.0 μmol / L to 50.0 μmol / L. While the release of high-potassium depolarization increased by 89.3% -332.1%, but also there are dose-effect relationship. Tip lead can not only promote glutamate neurotransmitter inactivation, but also interfere with its release process. This may affect the neurotransmitter synaptic transmission process and its excitatory effects, so that the LTP phenomenon weakened or unable to produce.