Neuropathic pain is chronic pain caused by damage of somatosensory system. However, existing analgesics are insufficient in effectiveness and have serious adverse effects. Although non-coding RNAs, especially microRNA, have been increasingly recognized as a critical modulator for neuropathic pain, involvement of long non-coding RNA (lncRNA) that is longer than 200 nucleotides is poorly understood. Here, we report a role of Neat1 lncRNA in the neuropathic pain. A rat neuropathic pain model was produced by ligation of the lumbar fifth spinal nerve. RNA sequencing of the dorsal root ganglion (DRG) revealed Neat1 was the most highly expressed among putative lncRNAs and was significantly upregulated in the injured DRG. Neat1 knockdown using AAV vector expressing shRNA alleviated mechanical allodynia and thermal hyperalgesia, and blocked expression changes in multiple genes related to inflammatory process or neuronal function. Many of these mRNAs were predicted to interact directly with Neat1. Neat1 knockdown in the DRG suppressed spinal microglial activation and elevated expressions of several pro-inflammatory cytokines after nerve injury. Neat1 may contribute to neuroinflammation in neuropathic pain through direct and indirect interaction with inflammatory genes.