首页> 外文期刊>Journal of neurogenetics >Type II phosphatidylinositol 4-kinase regulates nerve terminal growth and synaptic vesicle recycling
【24h】

Type II phosphatidylinositol 4-kinase regulates nerve terminal growth and synaptic vesicle recycling

机译:II型磷脂酰肌醇4-激酶调节神经末端生长和突触囊泡再循环

获取原文
获取原文并翻译 | 示例
       

摘要

Type II phosphatidylinositol 4-kinase (PI4KII) is thought to be associated with synaptic vesicles (SVs) and to be responsible for the majority of PI4K activity in the nervous system. However, the function of PI4KII at the synapse is unknown. We characterized the synaptic phenotypes of a Drosophila melanogaster PI4KII null mutant. We found increased nerve terminal growth in PI4KII null mutants indicating that PI4KII restrains nerve terminal growth. Evoked neurotransmitter release elicited in response to low frequency stimulation and spontaneous neurotransmitter release were not altered in PI4KII null mutants. However, PI4KII null mutants displayed reduced FM1-43 uptake in response to stimulation by high K+ saline, indicating impaired SV endocytosis. PI4KII null mutants did not display any defects in FM1-43 unloading, consistent with normal SV exocytosis. Thus, PI4KII is required for SV endocytosis but dispensable for SV exocytosis. Overall, our data show that PI4KII regulates both nerve terminal growth and SV recycling.
机译:II型磷脂酰肌醇4-激酶(PI4KII)被认为与突触囊泡(SV)相关,并负责神经系统中的大多数PI4K活性。但是,PI4kii在突触处的功能是未知的。我们表征了果蝇Melanogaster pi4kii null突变体的突触表型。我们发现PI4KII NULL突变体中的神经末端生长增加,表明PI4KII抑制神经末端生长。诱发的神经递质释放响应低频刺激和自发性神经递质释放释放,在PI4KII NULL突变体中没有改变。然而,PI4KII NULL突变体响应于高K +盐水刺激而显示出降低的FM1-43摄取,表明SV内吞作用受损。 PI4KII NULL突变体没有显示FM1-43卸载中的任何缺陷,符合正常的SV外尿量。因此,SV内吞作用需要PI4KII,但是对于SV外尿作用的可分配。总体而言,我们的数据表明,PI4KII调节神经终端生长和SV回收。

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