Modulation of premotor cortex excitability mitigates the behavioral and electrophysiological abnormalities in a Parkinson's Disease Mouse Model

Our study provides insight into the mechanisms underlying motor impairment in Parkinson's disease (PD) and the therapeutic effect of deep brain stimulation (DBS). By elucidating the role of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in modulating the hyperexcitability of M2 neurons, we identify potential targets for future PD treatment strategies. Understanding the excessive excitability and suppressive motor control through M2-STN synapses in PD mouse models contributes to our knowledge of circuit-level dynamics underlying DBS effects. These findings have significant implications for improving motor symptoms and advancing the development of more precise and effective interventions for PD patients.