铅对大鼠海马谷氨酸递质体外摄取和释放的影响

Influence of Lead on the Uptake and Release of ~3H-DL-glutamate in the Rat Hippocampal Synaptosomes and Slices

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。

To investigate the mechanism of lead-induced impairment in learning and memory function,the effects of lead on glutamate uptake and release in rat hippocampal synaptosomes and slices were respechvely studied in vitro. The results showed that exposure to 3. 1 ~ 50. 0μmol/L lead produced a dose -dependent increase in glutamate uptake into the synaptosomes by 70. 4% ~ 193. 2% and in the spontaneous release from the slices by 23. 2% ~ 66. 2% in the absence of calcium. However, in the presence of calcium, lead was added from 1. 0 to 50. 0μmolus, increased potassium evoked the release by 89. 3 %~332. 1 % and attenuated the spontaneous release by 22.6% ~ 55 .3% in the preloaded slices with a concentration-dependent manner. The present results indicated that lead may facilitate the inactivation of glutamate neurotrgnsmitter and interfere with its release process, resulting in the alterations of glutamate neurtransmission in synapses. These may further lead to the inhibition of excitatory actions of the transmitter with a reduction or abortion of LTP in synapses.