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Background Inflammatory pain is a severe clinical problem that affects the quality of life in patients. However, the currently available treatments for inflammatory pain have limited effect and even causes severe side effects. The aim of this study was to investigate the roles of miRNA‐107 and glutamate transporter 1 (GLT‐1) in the inflammatory pain of rats induced by complete Freund's adjuvant (CFA). Methods Paw withdrawal threshold (PWT) of rats was measured by von Frey Filaments. The expressions of miRNA‐107 and GLT‐1 in the lumbar spinal dorsal horn (L4‐L6) were measured with real‐time quantitative PCR and western blotting analysis. Fluorescent in situ hybridization and fluorescent‐immunohistochemistry were employed to detect the expression of miRNA‐107, GLT‐1 and co‐location of miRNA‐107 with GLT‐1. Results Injection of CFA significantly reduced PWT of rats. The miRNA‐107 expression level was obviously up‐regulated while the GLT‐1 expression level was decreased in the spinal dorsal horn of CFA rats. miRNA‐107 and GLT‐1 were co‐expressed in the same cells of the spinal dorsal horn in CFA rats. Ceftriaxone, a selective activator of GLT‐1, obviously increased the PWT of CFA rats. Furthermore, antagomir of miRNA‐107 reversed the down‐regulation of GLT‐1 and alleviated CFA‐induced mechanical allodynia of CFA rats. Conclusions These results suggest that an increase of miR‐107 contributes to inflammatory pain through downregulating GLT‐1 expression, implying a promising strategy for pain therapy. Significance The currently available treatments for inflammatory pain has limited effect even causes severe side effects. MiRNAs may have important diagnostic and therapeutic potential in inflammatory pain. In present study, we show a potential spinal mechanism of allodynia in rat inflammatory pain model induced by CFA. Increased miR‐107 contribute to inflammatory pain by targeting and downregulating GLT‐1 expression, implying a promising strategy for inflammatory pain.