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TRPC3‐dependent synaptic transmission in central mammalian neurons

  • Technische Universität München
  • Munich Cluster for Systems Neurology (SyNergy)

Publikation: Beitrag in Fachzeitschrift › Übersichtsartikel › Begutachtung

25 Zitate (Scopus)

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.

OriginalspracheEnglisch
Seiten (von - bis)983-989
Seitenumfang7
FachzeitschriftJournal of Molecular Medicine
Jahrgang93
Ausgabenummer9
DOIs
PublikationsstatusVeröffentlicht - 26 Sept. 2015

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