Parkinson's disease (PD) is characterized by increased $\beta$-band (13–30 Hz) synchronization. Although previous studies have indicated that the striatum plays a crucial part in generating and transmitting the $\beta$-band oscillations, the underlying biophysical basis remains unclear. An extended thalamic–basal ganglia (BGTC) model including the striatum (BGSTC) is used to examine the striatal influence on $\beta$-band synchronous oscillations in the globus pallidus pars interna (GPi). This influence is implemented by modulating striatal inhibitory input. Phase-locking value (PLV) and phase consistency (PC) show that the basal ganglia (BG) network exhibits pronounced $\beta$-band synchrony in the Parkinsonian state. Moreover, enhancing striatal synaptic inputs may induce $\beta$-band desynchronization in GPi via the direct pathway. In contrast, the modulation via the indirect pathway has a much weaker influence and may even exert an opposite effect. These conclusions not only reveal the striatum's regulatory capacity, but also provide a new avenue for PD therapy.