Deletion of the acid-sensing ion channel ASIC3 prevents gastritis-induced acid hyperresponsiveness of the stomach–brainstem axis

摘要: Gastric acid challenge of the rat and mouse stomach is signalled to brainstem as revealed by expression c-Fos. The molecular sensors relevant detection gastric mucosal acidosis are not known. Since acid-sensing ion channels ASIC2 ASIC3 expressed primary afferent neurons, we examined whether knockout or gene modifies signalling a insult in normal inflamed stomach. conscious mice (C57BL/6) was challenged with intragastric HCl; two hours later activation neurons nucleus tractus solitarii (NTS) visualized c-Fos immunocytochemistry. Mild gastritis induced addition iodoacetamide (0.1%) drinking water for 7 days. Exposure mucosa HCl (0.25 M) caused 3-fold increase number c-Fos-positive NTS. This input NTS remained unchanged knockout, whereas augmented response 33% (P < 0.01). Pretreatment wild-type mild gastritis, increased myeloperoxidase activity, enhanced responding 41% hyperresponsiveness absent but fully preserved mice. current data indicate that plays major role associated experimental gastritis. In contrast, appears dampen acid-evoked from