Effects of tropicamide on catalepsy and motor function in a mouse model of Parkinson’s disease

JOURNAL/agad/04.03/02274129-202509000-00001/figure1/v/2025-06-20T105132Z/r/image-tiff Parkinson’s disease is a progressive disorder characterized by dopaminergic neuronal apoptosis in the basal ganglia. The prevalence of this condition increases with age. A key deficit in Parkinson’s disease is the loss of automaticity, which affects the patients’ daily activities. Levodopa is the most effective treatment for Parkinson’s disease. However, because it is not effective for all patients in later stages of the disease, new approaches have been proposed. This study investigated the effects of tropicamide, an M4 muscarinic receptor antagonist, on catalepsy and gait in an animal model of Parkinson’s disease. Two experiments were conducted. In both experiments, animals were injected with either haloperidol to induce Parkinson’s disease-like symptoms or saline as a placebo for the control group. In Experiment I, animals received an intraperitoneal injection of either tropicamide (the experimental intervention) or saline (the placebo). In Experiment II, tropicamide or saline was administered intracerebrally instead of intraperitoneally. Catalepsy was assessed using the Bar Test and gait was evaluated using the open field test. Haloperidol induced catalepsy and motor impairments resembling those observed in Parkinson’s disease. Tropicamide administration, both intraperitoneally and intracerebrally, reversed haloperidol-induced deficits. These findings suggest that tropicamide can potentially mitigate Parkinson’s disease-related motor impairment. They also suggest a strong interaction between the M4 muscarinic receptors and dopaminergic pathways in the basal ganglia. These results underscore the importance of developing new pharmacological strategies targeting M4 muscarinic receptors in patients with Parkinson’s disease.