Reduced aspartate release from rat hippocampal synaptosomes loaded with Clostridial toxin light chain by electroporation: evidence for an exocytotic mechanism.
Reduced aspartate release from rat hippocampal synaptosomes loaded with Clostridial toxin light chain by electroporation: evidence for an exocytotic mechanism.
复制标题
通过电穿孔减少负载梭菌毒素轻链的大鼠海马突触体释放天冬氨酸：胞吐机制的证据。
DOI：
10.1016/j.neulet.2006.11.006
复制
发表时间：
2007
影响因子：
2.5
通讯作者：
Nadler,JVictor
中科院分区：
文献类型：
--
作者：
Wang,Lulu;Nadler,JVictor
天冬氨酸可与谷氨酸或GABA一起从某些海马通路沿着释放。虽然天冬氨酸免疫反应已被定位于突触囊泡和天冬氨酸释放是Ca2+依赖性的，一直没有明确的证据，有利于胞吐机制。特别是，用梭菌毒素预处理并不一致地抑制天冬氨酸的释放，即使当从相同的组织样品中释放谷氨酸被显著抑制时。为了直接解决这个问题，在存在活性或失活梭菌毒素轻链的情况下，通过电穿孔瞬时透化大鼠海马突触体。加载大鼠海马突触体与破伤风毒素或肉毒杆菌神经毒素A，B或C的活性轻链减少K+诱发的释放天冬氨酸至少一样多的谷氨酸。这些结果证实，在大鼠海马中天冬氨酸通过胞吐作用释放。
Aspartate can be released from certain hippocampal pathways along with glutamate or GABA. Although aspartate immunoreactivity has been localized to synaptic vesicles and aspartate release is Ca2+-dependent, there has been no clear evidence favoring an exocytotic mechanism. In particular, pretreatment with Clostridial toxins has not consistently inhibited aspartate release, even when release of glutamate from the same tissue samples was markedly inhibited. To address this issue directly, rat hippocampal synaptosomes were permeabilized transiently by electroporation in the presence of active or inactivated Clostridial toxin light chains. Loading rat hippocampal synaptosomes with the active light chain of tetanus toxin or of botulinum neurotoxins A, B or C reduced the K+-evoked release of aspartate at least as much as that of glutamate. These results confirm that aspartate is released by exocytosis in rat hippocampus.