首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >EVIDENCE FOR SYNAPTOTAGMIN AS AN INHIBITORY CLAMP ON SYNAPTIC VESICLE RELEASE IN APLYSIA NEURONS
【24h】

EVIDENCE FOR SYNAPTOTAGMIN AS AN INHIBITORY CLAMP ON SYNAPTIC VESICLE RELEASE IN APLYSIA NEURONS

机译:突触素作为抑制神经元突触囊泡释放的抑制物的证据

获取原文
获取原文并翻译 | 示例
           

摘要

While previous studies have demonstrated that synaptotagmin plays an essential role in evoked neurotransmitter release, it has been difficult to determine whether it acts to facilitate or inhibit release. To address this question, we used acute genetic manipulations to alter the expression of synaptotagmin in Aplysia neurons. Transient overexpression of synaptotagmin in acutely dissected cholinergic neurons and in cultured glutaminergic neurons decreased the amplitude of the excitatory postsynaptic potential (EPSP) by 32% and 26%, respectively. In contrast, treatment of cultured presynaptic neurons with synaptotagmin antisense oligonucleotides increased the amplitude of the EPSP by 50-75%. These results are consistent with a role of synaptotagmin as an inhibitor of release. [References: 31]
机译:尽管先前的研究表明突触结合素在诱发的神经递质释放中起着至关重要的作用,但很难确定其是促进还是抑制释放。为了解决这个问题,我们使用了急性遗传操作来改变海兔神经元中突触结合蛋白的表达。在急性解剖的胆碱能神经元和培养的谷氨酰胺能神经元中突触突触素的瞬时过表达分别使兴奋性突触后电位(EPSP)的幅度降低了32%和26%。相反,用突触突触素反义寡核苷酸处理培养的突触前神经元可使EPSP的幅度增加50-75%。这些结果与突触结合蛋白作为释放抑制剂的作用一致。 [参考:31]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号