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Abstract: Interstitial cells of Cajal (ICC), especially myenteric interstitial cells of Cajal (ICC‐MY), are key to gastrointestinal motility. However, their role in the pathogenesis of functional dyspepsia (FD) is unclear. Therefore, autophagy and differentiation of ICC‐MY were investigated to elucidate the pathogenesis of gastric motility disorder in FD. FD model was induced by chronic stress via tail clamping in rats, which was assessed by the vital signs of rats, gastric emptying rate result, and histology. The ultrastructure of ICC‐MY was examined using transmission electron microscope. In ICC‐MY, changes in autophagic biomarkers (Beclin1 and LC3B) and differentiation biomarkers (c‐kit and SCF) were evaluated with in situ hybridization, quantitative real time PCR, immunofluorescence, and Western blot, respectively. The FD model was successfully induced in rats, as evidenced by the abnormal vital signs (such as loss of appetite, liquid excreta, less activity, and slower weight gain), the decrease in gastric emptying rates, and little pathological change in gastric antrum tissue. Compared with the control group, FD caused increased organelle denaturation or reduction and increase in vacuolization. FD also promoted generation of autophagosomes in ICC‐MY. Moreover, increased the expression of Beclin1 and LC3B, but decreased expression of c‐kit and SCF. Excessive autophagy and abnormal differentiation of ICC‐MY may contribute to the pathogenesis of gastric motility disorder in FD. [ABSTRACT FROM AUTHOR]