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Handbook of Neurochemistry and Molecular Neurobiology pp 489–508Cite as

Signal Molecules and Calcium

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Abstract

The 28 mammalian members of the superfamily of transient receptor potential (TRP) channels are cation channels, mostly permeable to both monovalent and divalent cations, and can be subdivided into six main subfamilies: the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), and the TRPA (ankyrin) groups. TRP channels are widely expressed in a large number of different tissues and cell types and their biological roles appear to be equally diverse. In neurons of the peripheral and central nervous system, TRP channels may substantially contribute to neuronal excitation, neurotransmitter release, and calcium homeostasis. Some TRPs are involved in sensory functions such as temperature and pain perception and may help to regulate body temperature or to avoid tissue-damaging stimuli like noxious temperatures or irritating chemicals. Other TRPs appear to be intimately connected to G-protein-coupled receptors, thereby linking chemical signals such as hormones and neurotransmitters to membrane excitability. TRPs may even be involved in regulation of neurite length and growth cone morphology. In this chapter, we provide an overview of the impact of TRP channels on cellular calcium-dependent processes in mammalian neurons and identify several TRPs for which a causal pathogenic role might be anticipated.

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Abbreviations

ADPR:

ADP-ribose

AITC:

allyl isothiocyanate

DRG:

dorsal root ganglion

HEK:

human embryonic kidney

NCCa-ATP:

nonselective Ca2+-activated channel

NMDA-R:

NMDA receptors

OGD:

oxygen–glucose deprivation

OVLT:

organum vasculosum lamina terminalis

PAG:

periaqueductal gray

PIP2 :

phosphatidylinositol bisphosphate

PLC:

phospholipase C

PNS:

peripheral nervous system

ROCE:

receptor-operated calcium entry

TRP:

transient receptor potential

VACCs:

voltage-activated Ca2+ channels

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Acknowledgements

We thank T. Voets for helpful comments on the manuscript and all members of the lab for helpful suggestions and criticisms. This work was supported by grants from the Human Frontiers Science Program (HFSP Research Grant Ref. RGP 32/2004, DD, BN), Novartis (ND), the Belgian Federal Government, the Flemish Government, the Onderzoeksraad KU Leuven (GOA 2004/07, F.W.O G.0172.03, Interuniversity Poles of Attraction Program, Prime Ministers Office IUAP Nr.3P4/23), Excellentiefinanciering EF/95/010), and the German Academic Exchange Service (DAAD to N.D.).

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  1. N. Damann
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  2. D. D’hoedt
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  3. B. Nilius
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Editors and Affiliations

  1. Center for Neurochemistry, Nathan S. Kline Institute for Psychiatric Research, 10962, 140 Old Orangeburg Road, Orangeburg, New York, USA

    Abel Lajtha (Director) (Director)

  2. Group Director of Neuro-Developmental Disorder Research Group, RIKEN Brain Science Institute, 351-0198, 2-1 Hirosawa Wako-shi, Saitama, Japan

    Katsuhiko Mikoshiba

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© 2009 Springer Science+Business Media, LLC

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Damann, N., D’hoedt, D., Nilius, B. (2009). Signal Molecules and Calcium. In: Lajtha, A., Mikoshiba, K. (eds) Handbook of Neurochemistry and Molecular Neurobiology. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-30370-3_26

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