The 6-OHDA Parkinson's Disease Mouse Model Shows Deficits in Sensory Behavior

Parkinson's disease (PD) is characterized by the degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta, leading to dopamine depletion in the striatum and the hallmark motor symptoms of the disease. However, non-motor deficits, particularly sensory symptoms, often precede motor manifestations, offering a potential early diagnostic window. The impact of non-motor deficits on sensation behavior and the underlying mechanisms remain poorly understood. In this study, we examined changes in tactile sensation within a parkinsonian state by employing a mouse model of PD induced by 6-hydroxydopamine (6-OHDA) to deplete striatal DA. Leveraging the conserved mouse whisker system as a model for tactile-sensory stimulation, we conducted psychophysical experiments to assess sensory-driven behavioral performance during a tactile detection task in both the healthy and PD-like state. Our findings reveal a range of deficits across subjects following 6-OHDA lesion, including DA loss, motor asymmetry, weight loss, and varying levels of altered tactile sensation behavior. Behavioral changes ranged from no impairments in minor cases to isolated sensory-behavioral deficits in moderate cases and severe motor dysfunction in advanced stages. These results underscore the complex relationship between DA imbalance and sensory-motor processing, emphasizing the need for precise and multifaceted behavioral measurements to accurately capture the diverse manifestations of PD.