Activation of native TRPC3 cation channels by phospholipase D.

Journal article

In the mammalian nervous system, stimulation of G-protein-coupled type I glutamate receptors triggers various forms of neuronal plasticity, including cerebellar long-term depression and hippocampal long-term potentiation. Activation of these receptors in the cerebellum also leads to a slow excitatory postsynaptic current mediated by nonselective TRPC3 cation channels. How TRPC3 channels are opened is unknown, although it is widely thought that channel gating requires phospholipase C activation. Using the patch-clamp technique and immunohistochemistry in rat cerebellar slices, we show that metabotropic glutamate receptors activate TRPC3 channels through the small GTP-binding protein Rho and subsequent phospholipase D stimulation. TRPC3 channel gating is independent of phospholipase C activity. These results reveal a new mechanism for the gating of the ubiquitous TRPC3 channel and identify a key role for phospholipase D in the generation of the slow excitatory postsynaptic current in cerebellar Purkinje cells.

Authors: Glitsch, M

• Publication status: Published
• Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology
• Volume: 24
• Issue: 1
• Pages: 318-325
• Publication date: 2010-01-01
• DOI: 10.1096/fj.09-134973
• EISSN: 1530-6860
• ISSN: 0892-6638
• Language: English
• Keywords: Cell Line; Patch-Clamp Techniques; Rats; Calcium Signaling; Receptors, Metabotropic Glutamate; Recombinant Proteins; Immunohistochemistry; 1-Butanol; Excitatory Postsynaptic Potentials; rho GTP-Binding Proteins; Purkinje Cells; Ion Channel Gating; Phospholipase D; TRPC Cation Channels; Animals; Rats, Sprague-Dawley; Humans; Cerebellum; Transfection; Type C Phospholipases