Nav1.3 is a tetrodotoxin-sensitive voltage-gated sodium channel isoform encoded by SCN3A, the abnormal expression of which plays a crucial role in the generation of ectopic discharge, as well as being associated with allodynia and hyperalgesia. Using bioinformatics analysis, we showed that miR-30b-5p directly targets SCN3A. We aimed to explore whether miR-30b-5p can participate in trigeminal neuralgia (TN) in rats by regulating the expression of Nav1.3. The rat TN model was constructed through infraorbital nerve-chronic constriction injury (ION-CCI), which was verified by measuring the change in mechanical threshold and the expression of activating transcription factor 3 (a marker of nerve damage) in the trigeminal ganglia (TG). The expression of miR-30b-5p in postoperative TG was downregulated, whereas that of Nav1.3 was upregulated in rats subjected to ION-CCI. Overexpression of miR-30b-5p repressed the expression of Nav1.3 in TG and alleviated ION-CCI-induced TN. MiR-30b-5p targets to regulate the expression of SCN3A, thereby reducing or aggravating TN. Therefore, miR-30b-5p may be a novel therapeutic target for neuropathic pain.