TRPC3‐dependent synaptic transmission in central mammalian neurons

Jana Hartmann, Arthur Konnerth

Research output: Contribution to journalReview articlepeer-review

22 Scopus citations

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.

Original languageEnglish
Pages (from-to)983-989
Number of pages7
JournalJournal of Molecular Medicine
Volume93
Issue number9
DOIs
StatePublished - 26 Sep 2015

Keywords

  • Ataxia
  • Cerebellum
  • Purkinje cell
  • STIM1
  • mGluR1

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