期刊
NEURON
卷 59, 期 3, 页码 392-398出版社
CELL PRESS
DOI: 10.1016/j.neuron.2008.06.009
关键词
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资金
- Deutsche Forschungsgemeinschaft [HA 5388/1-1, IRTG 1373, GRK 333]
- Intramural Research Program of the NIH
- National Institute of Environmental Health Sciences [Z01-ES101684]
- Schiedel Foundation
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.
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