Basal ganglia (BG) circuits are crucial for motor initiation and suppression. Dopamine loss in these circuits triggers Parkinson's disease (PD) and debilitating motor impairments such as akinesia and bradykinesia. Levodopa treatments alleviates PD symptoms, but often leads to abnormal involuntary movements known as levodopa-induced dyskinesias (LIDs). Understanding the neuronal mechanism of LIDs is essential for developing novel therapeutic strategies. Recent studies suggest that LIDs result from abnormal striatal activity, yet how this activity affects downstream BG circuits to generate LIDs remains unknown. The external globus pallidus (GPe) integrates striatal inputs and serves as a hub to orchestrates both normal and pathological BG activity. Additionally, the striatal projections from arkypallidal GPe neurons form a negative feedback loop that control striatal action inhibition under normal conditions. However, their role in LIDs remains unknown.In this work, we first investigate the connectivity between arkypallidal neurons and the different striatal projection neurons using in vivo electrophysiological recordings and optogenetic manipulations. We then used in vivo miniscope imaging to monitor the change of calcium activity in arkypallidal neurons upon transition from normal to the different pathological motor states (PD vs. LIDs). We also verified how this change in calcium signal translates into spiking activity using in vivo electrophysiological recordings. Altogether, our data demonstrate a reduced activity of arkypallidal neurons during LIDs, which, if reversed by optogenetic intervention could reduce the severity of LIDs.This study elucidates the dysregulated activity of arkypallidal neurons in LIDs and highlights their potential as therapeutic targets for LIDs management.