期刊
SCIENTIFIC REPORTS
卷 5, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep11135
关键词
-
资金
- US National Institute on Aging [AG032320]
- Advancing a Healthier Wisconsin and Alzheimer's Association
- Research and Education Initiative Fund
- component of the Advancing a Healthier Wisconsin Endowment at the Medical College of Wisconsin
- National Center for Advancing Translational Sciences [8UL1TR000055]
Calmodulin (CaM) plays a key role in synaptic function and plasticity due to its ability to mediate Ca2+ signaling. Therefore, it is essential to understand the dynamics of CaM at dendritic spines. In this study we have explored CaM dynamics using live-cell confocal microscopy and fluorescence recovery after photobleaching (FRAP) to study CaM diffusion. We find that only a small fraction of CaM in dendritic spines is immobile. Furthermore, the diffusion rate of CaM was regulated by neurogranin (Ng), a CaM-binding protein enriched at dendritic spines. Interestingly, Ng did not influence the immobile fraction of CaM at recovery plateau. We have previously shown that Ng enhances synaptic strength in a CaM-dependent manner. Taken together, these data indicate that Ng-mediated enhancement of synaptic strength is due to its ability to target, rather than sequester, CaM within dendritic spines.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据