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First published online on July 14, 2004.
 Copyright © 2004 by The Physiological Society
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Received March 26, 2004
Revised May 4, 2004
Accepted after revision July 9, 2004

Human TRPC5 channel activated by a multiplicity of signals in a single cell

Fanning Zeng1, Shang-Zhong Xu1, Philippa K Jackson1, Damian McHugh1, Bhaskar Kumar1, Samuel J Fountain1, and David J Beech1*

1 University of Leeds

* To whom correspondence should be addressed. E-mail: d.j.beech{at}leeds.ac.uk.

Here we explore the activation mechanisms of human TRPC5, a putative cationic channel that was cloned from a region of the X chromosome associated with mental retardation (Sossey-Alaoui et al., 1999). No basal activity was evident but activity was induced by carbachol stimulation of muscarinic receptors independently of calcium release. This is "receptor-activation", as described for mouse TRPC5. In addition, and in the absence of receptor stimulation, extracellular 0.1 mM gadolinium activated TRPC5, an effect that was mimicked by 5-20 mM external calcium with intracellular calcium buffered. We refer to this as "external ionic-activation". TRPC5 was also activated by modest elevation of the intracellular calcium concentration in the absence of GTP - "calcium-activation". A putative fourth activation mechanism is a signal from depleted intracellular calcium stores. Consistent with this idea, human TRPC5 was activated by a standard store-depletion / calcium re-entry protocol, an effect that was difficult to explain by calcium activation. Multiplicity of TRPC5 activation was demonstrated in single cells and thus not explained by heterogeneity of expression levels or cellular context. Therefore, human TRPC5 is activated by a range of stimuli, avoiding dependence on a single critical activator like many other ion channels. One of these stimuli would seem to be a change in calcium-handling by the endoplasmic reticulum.


Key words: Calcium channel • Calcium entry • Membrane current




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