Insomia is a common problem for people with chronic pain. Nociceptive information is transmitted by a neuronal pathway that projects from the thalamus to the so-called pain matrix, including the somatosensory cortex and the anterior cingulate cortex (ACC). In our previous study, we demonstrated that neuropathic pain decreased the level of GABA released at the synaptic cleft in the mouse ACC associated with an increase in GABA uptake through increased GABA transporters (GATs) on astrocytes, which results in the suppression of GABAergic transmission in the ACC region. However, the role of the astrocytes in the ACC under the chronic pain has been yet to be elucidated fully. In this study, we investigated whether activated-astrocytes in the ACC region could be associated with sleep dysregulation related to pain behaviors. We confirmed that sciatic nerve ligation caused thermal hyperalgesia and tacticle allodynia in mice. Mild noxious heat stimuli significantly increased the release of glutamate in the ACC of nerve ligated-mice compared to that of sham-operated mice. In addition, sciatic nerve-ligation and mild noxious stimuli changed the morphology of astrocytes in the ACC. In an experiment with primary cultured glial cells from the mouse cortex, treatment of glutamate caused astrocytic activation, as detected by a stellate morphology. Furthermore, glutamate induced the translocation of GATs to astrocyte cell membranes. Moreover, the GABA level at the synaptic cleft in the ACC of nerve ligated-mice was significantly decreased by exposure to mild noxious stimuli. Currently, we investigated whether astrocyte activation in the ACC could directly induce the changes in sleep. Using an optogenetic tool with channel rhodopsin-2, we demonstrated that selective photostimulation of glial fibrillary acidic protein-positive astrocytes in vivo triggered sleep disturbance. These approaches provide novel evidences that astrocytic activation in the ACC may, at least in part, explain the sleep disturbance with chronic pain.