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Background Bone cancer patients are often accompanied with pain and depression, which seriously affects their quality of life and survival time. Fluoxetine, a selective serotonin reuptake inhibitor, has been reported to be effective not only in reducing depression-like behaviors but also in alleviating cancer pain. However, the specific mechanisms involved remain obscure. Methods Bone cancer mice were treated with fluoxetine for 7 consecutive days after the formation of pain and depression symptoms. Neuroinflammation and synaptic changes at the basolateral amygdala (BLA) after treatment were examined with western blotting, immunofluorescence and Golgi-Cox staining. Results Compared with the tumor group, fluoxetine significantly improved the mechanical allodynia and sugar water preference ratio, and reduced the immobility time of forced swimming. In addition, we found fluoxetine had an inhibitory effect on reactive glial cells and neurotoxic glial cells of bone cancer pain (BCP) mice. Meanwhile, fluoxetine could improve synaptic function in the bone cancer mice basolateral amygdala regions. Conclusions Fluoxetine can effectively alleviate pain-like and depression-related behaviors in BCP model. The concerned mechanisms may be related to reducing neurotoxic glial cells activation and promoting synapse formation at BLA.