The number of patients suffering from chronic pain is increasing rapidly in adult demographics. Neuropathic pain- associated social disorders (NPSD) lack adequate attention, despite having a significantly impact on patients' quality-of-life. We found that the mouse model of neuropathic pain elicits significant NPSD, accompanied by an increased number of astrocytes in the anterior cingulate cortex (ACC). Inhibition of ACC astrocytes by pharmacological or chemogenetic method could reverse NPSD in SNI mice. Meanwhile, fMRI, in vivo electrophysiological recording and chemogenetics identified ACC-CPu as a neural circuit underlying NPSD. In addition, we analyzed cell types and differential genes in ACC using single-cell sequencing, and found that NPSD caused upregulation of astrocyte-derived Sparc, a protein implicated in synaptogenesis, in the ACC of SNI mice. Our understanding of the pathologic process of this psychological disorder may provide suggestions for the development of appropriate clinical intervention strategies, and therefore lay a foundation for improving the quality of life of patients with chronic pain.