Neuropathic pain is intractable chronic pain caused by damage to somatosensory systems. Recently, microRNAs, small non-coding RNAs modulating translation of specific genes, have been shown to be involved in a broad range of neuronal disorders including neuropathic pain. miR-17-92 is a polycistronic microRNA cluster comprising six distinct mature microRNAs, namely miR-17, miR-18a, miR-19a, miR-19b, miR-20a and miR-92a, on a single transcript. In the neuropathic pain state, our previous microRNA microarray results showed that all the members of miR-17-92 cluster were upregulated in the dorsal root ganglion (DRG). Here, we examined the involvement of miR-17-92 cluster in the neuropathic pain state induced by the fifth lumbar (L5) spinal nerve ligation in rats. Quantitative RT-PCR revealed that expressions of all the miR-17-92 cluster members were significantly increased in the L5 DRG 3 days after the nerve injury, and reached a peak at day 7. The increase in microRNA expressions persisted for at least 14 days. Primary miR-17-92, but not its paralog miR-17-363, was also upregulated in the L5 DRG in a similar time course to the mature miRNAs. On the other hand, the expression of miR-17-92 cluster members was unchanged in inflammatory pain induced by complete Freund's adjuvant. To investigate the miR-17-92 involvement in the pain-related behaviors, the miR-17-92 cluster was overexpressed in the L5 DRG of intact rats using adeno-associated virus vector. The miR-17-92 cluster overexpression caused mechanical allodynia as observed in the neuropathic pain state. These results suggest that miR-17-92 cluster upregulation in the DRG may be causally involved in neuropathic pain and provide a potential target for effective management of neuropathic pain.