TRPC3 channels are required for synaptic transmission and motor coordination

被引：325

作者：

Hartmann, Jana ^{[1
,2
]}

Dragicevic, Elena ^{[1
,2
]}

Adelsberger, Helmuth ^{[1
,2
]}

Henning, Horst A. ^{[1
,2
]}

Sumser, Martin ^{[1
,2
]}

Abramowitz, Joel ^{[3
]}

Blum, Robert ^{[4
]}

Dietrich, Alexander ^{[5
]}

Freichel, Marc ^{[6
]}

Flockerzi, Veit ^{[6
]}

Birnbaumer, Lutz ^{[3
]}

Konnerth, Arthur ^{[1
,2
]}

机构：

[1] Tech Univ Munich, Inst Neurosci, D-80802 Munich, Germany

[2] Tech Univ Munich, Ctr Integrated Prot Sci, D-80802 Munich, Germany

[3] NIEHS, Transmembrane Signaling Grp, Res Triangle Pk, NC 27709 USA

[4] Univ Munich, Inst Physiol, D-80336 Munich, Germany

[5] Univ Marburg, Inst Pharmacol & Toxicol, D-35043 Marburg, Germany

[6] Univ Saarland, Inst Expt & Clin Pharmacol & Toxicol, D-66421 Homburg, Germany

来源：

NEURON | 2008年 / 59卷 / 03期

关键词：

D O I：

10.1016/j.neuron.2008.06.009

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In the mammalian central nervous system, slow synaptic excitation involves the activation of metabotropic glutamate receptors (mGluRs). It has been proposed that C1-type transient receptor potential (TRPC1) channels underlie this synaptic excitation, but our analysis of TRPC1-deficient mice does not support this hypothesis. Here, we show unambiguously that it is TRPC3 that is needed for mGluR-dependent synaptic signaling in mouse cerebellar Purkinje cells. TRPC3 is the most abundantly expressed TRPC subunit in Purkinje cells. In mutant mice lacking TRPC3, both slow synaptic potentials and mGluR-mediated inward currents are completely absent, while the synaptically mediated Ca2+ release signals from intracellular stores are unchanged. Importantly, TRPC3 knockout mice exhibit an impaired walking behavior. Taken together, our results establish TRPC3 as a new type of postsynaptic channel that mediates mGluR-dependent synaptic transmission in cerebellar Purkinje cells and is crucial for motor coordination.

引用

页码：392 / 398

页数：7

共 38 条

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