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However, the role and potential mechanisms of EA in PD\u2010associated depression remain unclear. In the present study, a rat model of PD with unilateral 6\u2010hydroxydopamine (6\u2010OHDA) lesions in the medial forebrain bundle was treated using EA for 4 weeks. We found that 100\u2009Hz EA improved several motor phenotypes. In addition, tyrosine hydroxylase (TH) immunohistochemical analysis showed that EA had a minimal impact on the TH\u2010positive profiles of the ipsilateral ventral tegmental area. Compared with the 6\u2010OHDA group, long\u2010term EA stimulation significantly increased sucrose solution consumption and decreased immobility time in the forced swim test. EA treatment did not alter dopamine, norepinephrine, and serotonin levels in the striatum and hippocampus. Noticeably, EA treatment reversed the 6\u2010OHDA\u2010induced abnormal expression of brain\u2010derived neurotrophic factor (BDNF) and tropomyosin\u2010related kinase B (TrkB) in the midbrain and hippocampus. These results demonstrate that EA at 100\u2010Hz possesses the ability to improve depressive\u2010like symptoms in PD rats, which is, at least in part, due to the distinct effect of EA on the mesostriatal and mesocorticolimbic dopaminergic pathways. 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