Gamma oscillations in basal ganglia stem from the interplay between local inhibition and beta synchronization

Abstract Basal ganglia rhythms have mainly been studied in the beta band (12–30 Hz), a hallmark of Parkinson’s disease (PD), while gamma oscillations (30–100 Hz) in the subthalamic nucleus (STN) have emerged as alternative markers for guiding adaptive deep brain stimulation. However, their underlying mechanisms remains unclear. Using a spiking network model of the basal ganglia, we identified two distinct gamma rhythms: a high-frequency gamma in pallidal (GPe-TI) neurons and a slower gamma in D2 medium spiny neurons (MSNs), both generated through self-inhibition. Under simulated parkinsonian condition, GPe-TI gamma intensity remained stable. In contrast, D2 MSN gamma emerged only in pathological conditions and was strongly modulated by beta activity in both intensity and frequency. Although STN did not generate gamma oscillations directly, gamma activity from GPe-TI population was reflected in simulated STN local field potentials. These results clarify the circuit origins of gamma rhythms and their modulation in PD. Competing Interest Statement The authors have declared no competing interest. Footnotes This version of the manuscript has been revised to include an additional figure in the main text to further substantiate the conclusions drawn.