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TRPC3 channels are required for synaptic transmission and motor coordination.

Neuron | Aug 14, 2008

http://www.ncbi.nlm.nih.gov/pubmed/18701065

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.

Pubmed ID: 18701065 RIS Download

Mesh terms: 6-Cyano-7-nitroquinoxaline-2,3-dione | Animals | Behavior, Animal | Calcium | Cerebellum | Electric Stimulation | Excitatory Amino Acid Agonists | Excitatory Amino Acid Antagonists | Excitatory Postsynaptic Potentials | In Vitro Techniques | Methoxyhydroxyphenylglycol | Mice | Mice, Knockout | Nerve Tissue Proteins | Neural Pathways | Patch-Clamp Techniques | Psychomotor Performance | Purkinje Cells | Synaptic Transmission | TRPC Cation Channels

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Associated grants

  • Agency: Intramural NIH HHS, Id: Z01 ES101684-05
  • Agency: NIEHS NIH HHS, Id: Z01-ES101684

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