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J Physiol Volume 572, Number 1, 165-172, April 1, 2006 DOI: 10.1113/jphysiol.2005.102889
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Rapid Report

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

Hui Hui1, Damian McHugh2, Meredith Hannan3, Fanning Zeng2, Shang-Zhong Xu2, Saeed-ul-Hassan Khan1, Robert Levenson3, David J. Beech2 and Jamie L. Weiss1

1 Biomedical Science, University of Sheffield, Sheffield S10 2TN, UK
2 Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK
3 Department of Pharmacology, Penn State College of Medicine, Hershey, PA 17033, USA

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.

(Received 2 December 2005; accepted after revision 2 February 2006; first published online 9 February 2006)
Corresponding author D. J. Beech: Institute of Membrane and Systems Biology, Garstang Building, University of Leeds, Leeds LS2 9JT, UK. Email: d.j.beech{at}leeds.ac.uk

Hui Hui and Damian McHugh contributed equally to this work.




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