Role of acid-sensing ion channel 3 in sub-acute-phase inflammation.

摘要: Inflammation-mediated hyperalgesia involves tissue acidosis and sensitization of nociceptors. Many studies have reported increased expression acid-sensing ion channel 3 (ASIC3) in inflammation enhanced ASIC3 activity with pro-inflammatory mediators. However, the role remains inconclusive because conflicting results generated from knockout (ASIC3-/-) or dominant-negative mutant mice, which shown normal, decreased during inflammation. Here, we tested whether plays an important subcutaneous paw muscle ASIC3-/- mice induced by complete Freund's adjuvant (CFA) carrageenan investigating behavioral pathological responses, as well profile channels. Compared ASIC3+/+ controls, showed normal thermal mechanical acute (4-h) intraplantar CFA- carrageenan-induced inflammation, but hyperalgesic effects sub-acute phase (1–2 days) were milder all paradigms except for CFA-induced Interestingly, primary was accompanied ASIC3-dependent Nav1.9 up-regulation increase tetrodotoxin (TTX)-resistant sodium currents. CFA-inflamed did not evoke whereas abolished previously described. attenuated features such less granulomas carrageenan-evoked vasculitis compared mice. We provide a novel finding that participates maintenance sub-acute-phase mediates process granuloma formation intramuscular