| First Author | Gomis A | Year | 2008 |
| Journal | J Physiol | Volume | 586 |
| Issue | 23 | Pages | 5633-49 |
| PubMed ID | 18832422 | Mgi Jnum | J:176563 |
| Mgi Id | MGI:5292203 | Doi | 10.1113/jphysiol.2008.161257 |
| Citation | Gomis A, et al. (2008) Hypoosmotic- and pressure-induced membrane stretch activate TRPC5 channels. J Physiol 586(Pt 23):5633-49 |
| abstractText | Transient receptor potential (TRP) channels mediate a wide array of sensory functions. We investigated the role of TRPC5, a poorly characterized channel widely expressed in the central and peripheral nervous system, as a potential osmosensory protein. Here we show that hypoosmotic stimulation activates TRPC5 channels resulting in a large calcium influx. The response to osmotically induced membrane stretch is blocked by GsMTx-4, an inhibitor of stretch activated ion channels. Direct hypoosmotic activation of TRPC5 is independent of phospholipase C function. However, the osmotic response is inhibited in a cell line in which PIP(2) levels are reduced by regulated overexpression of a lipid phosphatase. The response was restored by increasing intracellular PIP(2) levels through the patch pipette. The mechano-sensitivity of the channel was probed in the whole-cell configuration by application of steps of positive pressure through the patch pipette. Pressure-induced membrane stretch also activated TRPC5 channels, suggesting its role as a transducer of osmo-mechanical stimuli. We also demonstrated the expression of TRPC5 in sensory neurones which together with the osmo-mechanical characteristics of TRPC5 channels suggest its putative role in mechanosensory transduction events. |
