Objective: To determine the expression of acid-sensing ion channel 3 (AsIc3) in esophageal mucosa and dorsal root ganglion(DRG) in rats with gastroesophageal reflux disease(GERD), and to explore its role in the pathogenesis of GERD. Methods: Male Sprague-Dawley rats were randomly divided into two groups: experimental group (G group) and control group (S group). The fundus of stomach of G group was ligated and the pylorus was restricted to establish GERD model. All the rats were sacrificed on day 15, the histopathology of sophgeal mucosa was observed, the expression of acid-sensing ion channel 3 (AIC3) protein and mRNA in esophageal mucosa and DRG were determined by Western blotting and real-time polymerase chain reaction (RT-PCR). Results: HE staining showed that chronic inflammatory changes were found in regions of esophgeal mucosa in G group where as normal in S group. Western blotting showed that the expression of ASIC3 protein in DRG was up-regulated in G group than that in S group(6.75±0.74 vs 5.07±0.72) (P<0.05)，and the expression of ASIC3 protein of esophageal mucosa was increased in G group compared with S group(8.04±0.67 vs 7.31±0.740) (P<0.05)；RT-PCR showed that the expression of ASIC3 mRNA of DRG was up—regulated in G group than that in S group(0.00030±0.00003 vs 0.00013±0.00002) (P<0.05), the expression of ASIC3 mRNA of esophageal mucosa was increased in G group compared with S group(0.01073± 0.00231 vs 0.00088±0.0007)(P<0.05)．Conclusion: The up-regulated expression of ASIC3 in DRG and esophgeal mucosa of rats with gastroesophageal reflux indicate that ASIC3 involved in the pathogenesis of esophageal visceral hypersensitivity．