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Phospholipase C-Coupled Receptors and Activation of TRPC Channels

  • Chapter
Transient Receptor Potential (TRP) Channels

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 179))

Abstract

The canonical transient receptor potential (TRPC) cation channels are mammalian homologs of the photoreceptor channel TRP in Drosophila melanogaster. All seven TRPCs (TRPC1 through TRPC7) can be activated through Gq/11 receptors or receptor tyrosine kinase (RTK) by mechanisms downstream of phospholipase C. The last decade saw a rapidly growing interest in understanding the role of TRPC channels in calcium entry pathways as well as in understanding the signal(s) responsible for TRPC activation. TRPC channels have been proposed to be activated by a variety of signals including store depletion, membrane lipids, and vesicular insertion into the plasma membrane. Here we discuss recent developments in the mode of activation as well as the pharmacological and electrophysiological properties of this important and ubiquitous family of cation channels.

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Authors and Affiliations

  1. Laboratory of Signal Transduction, Department of Health and Human Services, National Institute of Environmental Health Sciences—NIH, Research Triangle Park, PO Box 12233, NC, 27709, USA

    M. Trebak, L. Lemonnier, J. T. Smyth, G. Vazquez & J. W. Putney Jr.

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  1. M. Trebak
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  2. L. Lemonnier
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  3. J. T. Smyth
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  4. G. Vazquez
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  5. J. W. Putney Jr.
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Editors and Affiliations

  1. Experimentele und Klinische, Pharmakologie und Toxikologie, Universität des Saarlandes, Gebäude 46, 66421, Homburg, Deutschland

    Veit Flockerzi

  2. Laboratorium voor Fysiologie, Katholieke Universiteit Leuven, Campus Gasthuisberg, Herestraat 49, 3000, Leuven, België

    Bernd Nilius

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Trebak, M., Lemonnier, L., Smyth, J.T., Vazquez, G., Putney, J.W. (2007). Phospholipase C-Coupled Receptors and Activation of TRPC Channels. In: Flockerzi, V., Nilius, B. (eds) Transient Receptor Potential (TRP) Channels. Handbook of Experimental Pharmacology, vol 179. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-34891-7_35

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