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Highlights • Behavioral analysis demonstrated that the CPSP animals displayed a significant decrease in mechanical allodynia threshold. • A significant increase in P2 × 4 receptors expression in microglia in thalamic peri-lesion tissues post-hemorrhage. • The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. • A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. • A significant decrease in P2 × 4 receptor expression after treatment with adrenergic antidepressants and antiepileptics. Abstract Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a significant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP. [ABSTRACT FROM AUTHOR]