<p>Enhanced beta oscillations (12–25 Hz) within the cortico-basal ganglia-thalamic network are significantly associated with motor deficits and are a prominent characteristic of the neural dynamic pathology in Parkinson’s disease. Although the striatum has been proposed as a promising origin for enhanced beta oscillations, the precise mechanism through which distinct striatal neurons collaborate to orchestrate beta oscillations remains elusive. This study constructs a biophysical neural network model of the striatum based on experimental constraints. The model faithfully reproduces various experimental observations, including dopamine-dependent beta oscillations and phase-locked firing patterns. Through both theoretical and numerical analysis, our analysis reveals that striatal beta oscillations emerge from interactions within the cellular architecture, particularly the somatostatin-expressing interneurons (SOM) driven choline acetyltransferase-expressing interneurons (ChAT)—indirect pathway striatal projection neurons (iSPN) loop. Our results underscore the critical role of ChATs in enhancing beta oscillations. ChATs, instead of passively providing excitatory drive, actively amplify beta oscillations by enhancing their excitation efficacy through a phase-locked mode. Additionally, the inhibitory interactions among iSPNs, with robust and slow inhibitory recovery dynamics within iSPNs, potentially result in beta oscillations. The slow inhibitory recovery is likely attributed to the slow dynamics of the KCNQ current. SOMs further modulate the beta oscillations by affecting their downstream ChAT–iSPN loop. These results provide novel insights into the mechanism underlying striatal beta oscillations, shedding light on the processes involved in beta oscillations generation during pathological states.</p>