Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to reduced striatal dopamine and motor and non-motor symptoms. The imbalance of adenosine signaling plays a role in the pathogenesis of PD, particularly through increased A2AR and reduced A1R activity affecting D2R and D1R signaling pathways, respectively. This imbalance interferes with the reciprocal modulation of adenylate cyclase by A1R/D1R and A2AR/D2R and impairs motor control. Despite existing treatment options, there is an unmet need for new interventions. Repetitive transcranial magnetic stimulation (rTMS) offers novel, non-invasive potential, but its underlying effects on PD remain to be fully understood. This study explores how prolonged intermittent theta burst stimulation (iTBS) modulates D1R-A1R and D2R-A2AR interaction in the 6-OHDA model of parkinsonism. Animals with unilateral 6-OHDA lesions underwent three weeks of iTBS. Motor skills were assessed using the rotarod test. Immunoblot, qRT-PCR, and immunohistochemistry analyses focused on adenosine and dopamine receptor signaling in the lesioned caudoputamen. iTBS significantly enhanced motor recovery post-6-OHDA lesion, with notable changes in receptor expression. A1R and D1DR levels increased, while A2AR and D2DR levels decreased, indicating a reversal of the pathological process. Our results showed that 6-OHDA-induced degeneration minimizes the expression of A1R and increase the expression of A2AR. iTBS offers a non-invasive method to counteract PD's dopaminergic and adenosinergic signaling imbalances, evidenced by restored receptor interaction and motor function recovery.