The involvement of ocular neuropathic pain in dry eye-induced chronic ocular pain has remained elusive. The aim of this study was to elucidate the mechanism for chronic ocular pain in dry eye model rats. The dry eye model was made by excision of the lacrimal gland (LGE) in 6-week-old SD rats. One week after the operation (1W), dry eye symptoms and hyperalgesia were developed on the LGE side. The corneal hyperalgesia on the LGE side persisted after the corneal damage was healed by treatment, thus suggesting the involvement of central sensitization. Therefore, we examined the glial cell activation in the trigeminal nucleus (Vi/Vc), where corneal sensory nerves project. The activation of microglia peaked at 1W on the LGE side. In contrast, astrocytes began to activate at 2W and continued to be activated thereafter. Since gabapentinoid, a ligand for the voltage-dependent Ca²⁺ channel α2δ subunit, has been reported to be effective on the ocular pain, we further investigated the expression of α2δ subunit in Vi/Vc. The signal intensity of α2δ subunit on the LGE side was significantly higher compared to the sham side at 1W and 8W. These results indicate that the dry eye causes ocular neuropathic pain by enhancing transmission of pain signal through the up-regulation of α2δ subunit and the activation of microglia and astrocytes in Vi/Vc.