Calcium-sensing mechanism in TRPC5 channels contributing to retardation of neurite outgrowth

被引：85

作者：

Hui, H

McHugh, D

Hannan, M

Zeng, FN

Xu, SZ

Khan, SUH

Levenson, R

Beech, DJ

Weiss, JL

机构：

[1] Univ Leeds, Inst Membrane & Syst Biol, Leeds LS2 9JT, W Yorkshire, England

[2] Univ Sheffield, Sheffield S10 2TN, S Yorkshire, England

[3] Penn State Coll Med, Dept Pharmacol, Hershey, PA 17033 USA

来源：

JOURNAL OF PHYSIOLOGY-LONDON | 2006年 / 572卷 / 01期

基金：

英国惠康基金;

关键词：

D O I：

10.1113/jphysiol.2005.102889

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The calcium- and sodium-permeable transient receptor potential channel TRPC5 has an inhibitory role in neuronal outgrowth but the mechanisms governing its activity are poorly understood. Here we propose a mechanism involving the neuronal calcium sensor-1 (NCS-1) protein. Inhibitory mutants of TRPC5 and NCS-1 enhance neurite outgrowth similarly. Mutant NCS-1 does not inhibit surface-expression of TRPC5 but generally suppresses channel activity, irrespective of whether it is evoked by carbachol, store depletion, lanthanides or elevated intracellular calcium. NCS-1 and TRPC5 are in the same protein complex in rat brain and NCS-1 directly binds to the TRPC5 C-terminus. The data suggest protein-protein interaction between NCS-1 and TRPC5, and involvement of this protein complex in retardation of neurite outgrowth.

引用

页码：165 / 172

页数：8

共 31 条

[1] Enhanced neurotransmitter release is associated with reduction of neuronal branching in a Drosophila mutant overexpressing frequenin [J].