In Parkinson's disease (PD), abnormal oscillations pervade the cortex–basal ganglia–thalamus (CTX-BG-Th) loop. In recent years, more and more evidence has shown the physiological phenomena of exaggerated phase–amplitude coupling (PAC) in PD, suggesting that such coupling contributes to the generation and propagation of pathological oscillations. However, current understanding of how cortical low-frequency rhythms shape downstream pathological activity is still incomplete. In this study, we aim to investigate how the theta-band (3–9 Hz) phase of layer 5 pyramidal tract (E5P) cortical neurons modulates the beta-band (13–30Hz) amplitude of globus pallidus internus (GPi) neurons. The modulation index (MI), time-lag MI analysis, and coherence analysis are introduced to quantify the strength, temporal characteristics, and pathway dependence of PAC. The results indicate that significant cross-regional $\theta$– $\beta$ PAC occurs between E5P and GPi in the PD state, and this coupling has time delay characteristics and mainly relies on indirect pathways. In addition, blocking indirect pathways or reducing the $\theta$ power of E5P will decrease the $\beta$ oscillation of GPi. These findings elucidate the dynamic mechanism of cortical regulation of GPi related oscillations, providing a theoretical basis for targeted interventions in PD patients through cortical modulation.

Pathological $\beta$-band oscillations (13–35 Hz) in the basal ganglia (BG) are strongly associated with Parkinson's disease (PD). Recent evidence shows that subpopulations of external globus pallidus (GPe) neurons exhibit distinct responses to pathological conditions, and that their inhibitory feedback to the striatum strongly shape BG dynamics, features often overlooked in conventional models. To address this, we developed an extended BG network using a modified Hodgkin–Huxley framework, incorporating two GPe subclasses, arkypallidal (TA) and prototypical (TI), along with striatal medium spiny neurons (MSNs) and fast-spiking interneurons (FSIs). Simulations revealed that mutual inhibition within the GPe drives TI neurons from tonic firing into $\beta$-bursting, retrogradely suppressing striatal activity through the GPe–FSI–MSN loop and disrupting direct/indirect pathway balance. We further show that GPe-TA projections exert strong inhibitory control over striatal populations, and that reducing MSN M-current reproduces $\beta$ oscillations that propagate downstream. Blocking D2 MSN $\to$ GPe-TI and GPe-TI $\to$ GPe-TA synapses restores normal TI firing. Our results emphasize the role of GPe heterogeneity in pathological oscillations and suggest circuit-level therapeutic strategies for PD.