| First Author | Sun H | Year | 2020 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 318 |
| Issue | 1 | Pages | L192-L199 |
| PubMed ID | 31664854 | Mgi Jnum | J:282950 |
| Mgi Id | MGI:6384307 | Doi | 10.1152/ajplung.00301.2019 |
| Citation | Sun H, et al. (2020) Role of TRP channels in Gq-coupled protease-activated receptor 1-mediated activation of mouse nodose pulmonary C-fibers. Am J Physiol Lung Cell Mol Physiol 318(1):L192-L199 |
| abstractText | We evaluated the mechanisms underlying protease-activated receptor 1 (PAR1)-mediated activation of nodose C-fibers in mouse lungs. The PAR1-induced action potential discharge at the terminals was strongly inhibited in phospholipase C-beta3 (PLCbeta3)-deficient animals. At the level of the cell soma, PAR1 activation led to an increase in cytosolic calcium that was largely inhibited by transient receptor potential (TRP) A1 antagonism. Patch-clamp recordings, however, revealed that neither TRPA1 nor TRPV1 or any other ruthenium red-sensitive ion channels are required for the PAR1-mediated inward current or membrane depolarization in isolated nodose neurons. Consistent with these findings, PAR1-mediated action potential discharge in mouse lung nodose C-fiber terminals was unaltered in Trpa1/Trpv1 double-knockout animals and Trpc3/Trpc6 double-knockout animals. The activation of the C-fibers was also not inhibited by ruthenium red at concentrations that blocked TRPV1- and TRPA1-dependent responses. The biophysical data show that PAR1/Gq-mediated activation of nodose C-fibers may involve multiple ion channels downstream from PLCbeta3 activation. TRPA1 is an ion channel that participates in PAR1/Gq-mediated elevation in intracellular calcium. There is little evidence, however, that TRPA1, TRPV1, TRPC3, TRPC6, or other ruthenium red-sensitive TRP channels are required for PAR1/Gq-PLCbeta3-mediated membrane depolarization and action potential discharge in bronchopulmonary nodose C-fibers in the mouse. |
