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Cell Calcium. 2010 Aug-Sep;48(2-3):124-32. doi: 10.1016/j.ceca.2010.07.006. Epub 2010 Aug 21.

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

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Department of Physiology, Hyogo College of Medicine, Mukogawa-cho, Nishinomiya, Japan.


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.

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