| First Author | Hartmann J | Year | 2008 |
| Journal | Neuron | Volume | 59 |
| Issue | 3 | Pages | 392-8 |
| PubMed ID | 18701065 | Mgi Jnum | J:139695 |
| Mgi Id | MGI:3809375 | Doi | 10.1016/j.neuron.2008.06.009 |
| Citation | Hartmann J, et al. (2008) TRPC3 channels are required for synaptic transmission and motor coordination. Neuron 59(3):392-8 |
| abstractText | 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. |
