Fibromyalgia (FM) is characterized by widespread musculoskeletal pain and tenderness, cognitive dysfunction, fatigue, and insomnia. The precise underlying mechanisms remain uncertain, hampering the development of specific curative therapies. Electroacupuncture (EA) has documented efficacy against FM-associated pain, while cannabinoid receptor 1 (CB1) plays a critical role in endogenous analgesia. Herein, we examined whether pain relief induced by EA is associated with altered cerebellar CB1 expression levels and signaling in the intermittent cold stress (ICS) mouse model of FM. Fibromyalgia-like pain and recovery were assessed by measuring mechanical and thermal pain thresholds. Compared to control mice, ICS-induced FM model mice exhibited a significantly reduced mechanical withdrawal threshold (2.29 0.13 g) and shorter thermal withdrawal latency (4.01 0.47 s), indicative of mechanical and thermal hyperalgesia. Both conditions were reversed by 2-Hz EA but not sham EA. Hyperalgesia was associated with reduced CB1 receptor expression and enhanced activity of multiple nociceptive signaling pathways (PKA, PI3K, Akt, mTOR, ERK, and NF-kB) in the mice cerebellum. 2-Hz EA but not sham EA reliably reversed these abnormalities. Intracerebroventricular injection of the CB1 agonist Anandamide (AEA) recapitulated the effects of EA on pain thresholds, while the analgesic effects of EA were blocked by the CB1 antagonist AM251. Our findings suggest that dysregulation of CB1 expression and aberrant hyperactivity of nociceptive signaling pathways in the cerebellum contribute to FM etiology and that upregulation of CB1 signaling mediates the analgesic efficacy of EA.