Background: Parkinsonism entails pronounced basal ganglia dysfunction, but emerging research suggests that broader subcortical networks, specifically the cerebellum, play a vital role in functional motor compensation following circuit-level destabilization. This study sought to characterize the electrophysiological dynamics of Multi-Unit Activity (MUA) amplitude in Crus II, the dentate nucleus (DN), and the inferior olive (IO) following a focal mechanical lesion of the ventrolateral striatum (VLS) as a circuit-level perturbation model during spontaneous behaviors. Methods: Bilateral mechanical VLS lesions were induced in 24 male Wistar rats. MUA signals were chronically recorded over a four-week protocol during self-grooming, horizontal locomotion, and rearing behaviors. Results: Crus II and the IO exhibited a structure-specific “dynamic transition,” shifting from early-stage hyperexcitability to significant late-stage attenuation by W4 (p < 0.001), reflecting a divergence from control trajectories rather than internal temporal drift within the lesioned state. Conversely, the DN showed sustained hypoactivity compared to healthy controls throughout the recording period (p < 0.05). Despite these robust neurophysiological shifts, the syntactic organization of grooming and exploratory patterns remained phenotypically preserved, indicating functional sufficiency despite underlying circuit noise. Conclusions: VLS injury triggers a rapid distributed reorganization across the striato-cerebellar network. The cerebellum acts as an active adaptive node, recalibrating internal network gain to mask early Parkinsonian-like circuit dysfunction at the level of functional sufficiency and maintain motor performance through active homeostatic gain regulation.
Viveros-Martínez et al. (Wed,) studied this question.