| Theme |
The Beginning of Neurogastroenterology |
| Title |
Role of Medullary TRH on Gastric Mucosal Injury |
| Author |
Hiroshi Kaneko |
Pathophysiology and Therapeutics, Aichi Medical University College of Nursing |
| Author |
Toshihiro Konagaya |
Department of Internal Medicine, Division of Gastroenterology, Aichi Medical University School of Medicine |
| Author |
Shinichi Kakumu |
Department of Internal Medicine, Division of Gastroenterology, Aichi Medical University School of Medicine |
| [ Summary ] |
Cold restraint stress (CRS) induced corpus mucosal erosions with hemorrhaging in rats. Aggressive factors, such as gastric acid, pepsin and high amplitude contractions have been reported to be responsible for gastric mucosal injury formation. Thyrotropin-releasing hormone (TRH) micro-injected into the cisterna magna or the dorsal motor nucleus (DMN) of the vagus (which contributes axons forming the gastric branch of the vagus) induced gastric injury similar to that seen with CRS and both were prevented by immuno-neutralization with TRH antibody injected centrally. These findings indicated that TRH on the DMN may contribute to CRS-induced gastric mucosal lesions. On the contrary, either exogenous or endogenous TRH at a sub-threshold dose increasing gastric acid secretion, alleviates gastric injury induced by intragastric administration of a strong irritant in rats. The dual action of TRH in the medulla on gastric integrity is mediated through activation of peripheral vagal-cholinergic pathways and the enteric nervous system. The outcome reflects the balance between aggressive factors such as gastric acid, and contractions and protective factors, including calcitonin gene-related peptide, nitric oxide and prostaglandins. The implications for medullary TRH actions obtained from animal experiments should be investigated in the pathogenesis of human gastric injury. |