Referenced in: none

Automatically associated channels: TRP , TRPM , TRPM8 , TRPV , TRPV1

Title: TRP channels are involved in mediating hypercapnic Ca2+ responses in rat glia-rich medullary cultures independent of extracellular pH.

Authors: Yutaka Hirata, Yoshitaka Oku

Journal, date & volume: Cell Calcium, 2010 Aug-Sep , 48, 124-32

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20728216

Abstract
The medulla contains central chemosensitive cells important for the maintenance of blood gas and pH homeostasis. To identify the intrinsic chemosensitive cells, we measured responses of intracellular Ca(2+) ([Ca(2+)](i)) and H(+) ([H(+)](i)), and membrane potential of rat primary-cultured medullary cells to 6-s exposure to acidosis. The cells showed transient [Ca(2+)](i) increases to extracellular pH 6.8, which was inhibited by the specific ASIC1a blocker (psalmotoxin-1), but did not respond to pH 7.1 in the HEPES-buffered solution. Isocapnic acidosis induced no changes in [Ca(2+)](i), whereas hypercapnic acidosis induced a remarkable Ca(2+) response and an increase in membrane potential in the HCO(3)(-)-buffered solution (pH 7.1). In glia-rich cultures, intracellular acidification preceded the hypercapnic acidosis-induced Ca(2+) response, and acetazolamide, a carbonic anhydrase inhibitor suppressed these responses. Transient receptor potential (TRP) channel broad-spectrum blockers Ni(2+) and ruthenium red, and a TRPV1- and TRPM8-specific blocker N-(4-tertiarybutylphenyl)-4-(3-chloropyridin-2-yl)-tetrahydropyrazine-1(2H)-carbox-amide attenuated the hypercapnic acidosis-induced Ca(2+) response. Subpopulations of cells that exhibited the hypercapnic acidosis-induced Ca(2+) response also responded to the application of capsaicin (TRPV1 agonist) and menthol (TRPM8 agonist). These results suggest that the TRP channel family partially mediates the fast hypercapnic acidosis-induced Ca(2+) response via changes in [H(+)](i) and is a candidate of central chemosensing proteins.