Modulating propagation of Parkinsonian beta oscillations with transcranial direct current stimulation: A computational study

Transcranial direct current stimulation (tDCS) is a non-invasive technique that primarily modulates cortical excitatory (E) neurons. Anodal tDCS targeting the motor cortex alleviates symptoms in Parkinson's disease patients, but the regulatory mechanisms remain obscure, especially for parkinsonian β band (13–30 Hz) oscillations. To explore these regulatory mechanisms, we propose a more refined model of the cortex-thalamic-basal ganglia (CTBG) neuronal network, with the primary issue of elucidating the impact of cortical neurons, as targets of tDCS, on parkinsonian β oscillations. Through blocking pathways, β oscillations in basal ganglia propagate to cortex mainly through thalamocortical connections, supplemented by direct connections from Lim homeobox 6 globus pallidus externa to cortical neurons. Simulations of two scenarios that lead to abnormal intracortical β band firing suggest that intracortical β band firing in healthy state is insufficient to drive β oscillations in CTBG circuit. This emphasizes the cortex as a critical node for the propagation and enhancement of β oscillations in CTBG circuit. To reveal the intrinsic regulatory mechanism of tDCS, different tDCS strategies targeting cortical E neurons are further compared. Anodal tDCS disrupts the abnormal oscillatory activity in CTBG circuits by promoting the activity of cortical neurons and interrupting oscillation propagation. In addition, anodic tDCS can amplify rhythmic activity within the afferent cortex, thereby concealing pathological oscillations. These findings provide a theoretical basis for understanding the role of cortex in parkinsonian oscillations and provide a conceptual platform for theoretical testing of tDCS for clinical applications.