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.
Citation: Quanbao Ji, Ruhu Lao. Effect of the striatum on $ \beta $-synchronous oscillatory activity[J]. Electronic Research Archive, 2026, 34(4): 2402-2418. doi: 10.3934/era.2026110
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.
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