Reconciling contradictory models of subthalamic nucleus contributions to basal ganglia beta oscillations

Recent computational studies of Parkinsons disease have yielded contradictory findings regarding the role of the subthalamic nucleus (STN) in pathological beta oscillations, with some models implicating STN as essential for beta generation and others suggesting that STN suppresses oscillations. This work addresses these discrepancies by systematically investigating how the specific features of the integrate-and-fire neurons used in these models influence simulated basal ganglia network dynamics. Using both rate models and spiking network simulations incorporating coupled subthalamopallidal and pallidostriatal circuits, we demonstrate that the choice between leaky integrate-and-fire (LIF) and quadratic integrate-and-fire (QIF) models to represent STN neurons fundamentally impacts the phase relationship between STN and external globus pallidus prototypical (Proto) neuron populations. QIF STN neurons establish in-phase coupling with Proto neurons, which enhances beta oscillation amplitude, while LIF STN neurons develop anti-phase relationships, which suppresses beta power. Through intervention experiments and parameter sweeps across physiologically relevant firing rates, we show that these phase-related effects persist robustly across network conditions, and we mathematically establish conditions under which these results are guaranteed to hold. Our findings reveal that the fundamental mathematical structure underlying spike generation, rather than other biophysical details, determines whether the subthalamopallidal loop acts as a beta amplifier or suppressor. This mechanistic insight reconciles contradictory findings in the literature, demonstrates that seemingly minor modeling choices can have profound consequences for understanding disease mechanisms and therapeutic targets, and offers predictions for determining which model framework reflects the biological reality. Author summarySubstantial work has explored the mechanisms underlying enhanced beta oscillations in the basal ganglia, motivated by their potential relevance to parkinsonian conditions and associated treatments. Often inferences about these mechanisms are based on simulations and reasoning that focus on features of network connectivity. We show that in fact the specific dynamical properties of the neurons in these circuits can strongly influence their emergent dynamics, with completely opposing effects arising in a given network structure depending on which neuron model is used, and we explain the factors underlying this divergence. Based on these factors, the determination of a small set of neuron properties in future biological experiments will lead to predictions about the mechanisms that can generate beta oscillations in the parkinsonian basal ganglia.