Spinal cord plasticity and acid-sensing ion channels involvement in a rodent model of irritable bowel syndrome

摘要: Irritable bowel syndrome (IBS) is a common functional gastro-intestinal disorder characterized by intractable chronic abdominal pain. In this study, we examined the possible spinal mechanisms underlying colonic hypersensitivity (CHS) using non-inflammatory rat model of IBS induced rectal enemas butyrate, short-chain fatty acid. We hypothesized that plasticity could be responsible for CHS and ASIC channels, which are known to support pain-elicited currents in cord, contribute central sensitization our IBS. First, order determine if visceral pain relies on changes activity, analyzed Fos expression cord rats treated with butyrate following challenge repetitive noxious colorectal distension. found immunoreactivity was increased thoracic T10–11–12, lumbar L1–2–6 sacral S1 segments. control saline, distensions evoked only Secondly, intrathecal injection PcTx1, specific ASIC1A antagonist, completely prevented development butyrate. ASIC1 2 mRNAs, especially ASIC1A, were upregulated cord. thus IBS, as it supported colocalization proteins. The whole data pinpoint potential critical role states such suggest channels part molecular effectors leading