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J Mol Med (Berl). 2015 Sep;93(9):983-9. doi: 10.1007/s00109-015-1298-7. Epub 2015 Jun 5.

TRPC3-dependent synaptic transmission in central mammalian neurons.

Author information

1
Institute of Neuroscience, Technische Universität München, Biedersteiner Str. 29, 80802, Munich, Germany. jana.hartmann@lrz.tum.de.
2
Munich Cluster for Systems Neurology (SyNergy) and Center for Integrated Protein Sciences (CIPSM), Munich, Germany. jana.hartmann@lrz.tum.de.
3
Institute of Neuroscience, Technische Universität München, Biedersteiner Str. 29, 80802, Munich, Germany.
4
Munich Cluster for Systems Neurology (SyNergy) and Center for Integrated Protein Sciences (CIPSM), Munich, Germany.

Abstract

The transient receptor potential (TRPC) proteins form non-selective cation channels that are activated downstream of Gq-phospholipase C-coupled receptors. TRPC3, one of the seven members of the TRPC subfamily, combines functions of an unspecific ion channel and a signal transducer. In the mammalian brain, the expression of TRPC3 is highest in cerebellar Purkinje cells, the principal neurons, and the sole output of the cerebellar cortex. In this review, we summarize findings identifying TRPC3 channels as integral components of glutamatergic metabotropic synaptic transmission. We give an overview of postsynaptic interaction partners and activation mechanisms of TRPC3 in central neurons. Finally, we address the deleterious consequences of distorted TRPC3 synaptic signaling for cerebellar function in different mouse models and present TRPC3 as an emerging candidate protein implicated in various forms of ataxia in humans.

KEYWORDS:

Ataxia; Cerebellum; Purkinje cell; STIM1; mGluR1

PMID:
26041382
DOI:
10.1007/s00109-015-1298-7
[Indexed for MEDLINE]

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