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.<br>

本研究阐明了帕金森病（PD）运动障碍的潜在机制，以及脑深部电刺激（DBS）的治疗效应。通过明确超极化激活环核苷酸门控（HCN）通道在调控M2神经元过度兴奋性中的作用，本研究确定了未来帕金森病治疗策略的潜在靶点。针对帕金森病小鼠模型中M2-丘脑底核突触介导的神经元过度兴奋性与运动控制抑制机制的解析，有助于深化我们对脑深部电刺激效应背后的环路级动力学特征的认知。上述研究发现对于改善帕金森病患者的运动症状，以及推动更精准有效的干预手段开发具有重要意义。