UCLA

The cerebral cortex is connected to various subcortical structures such as the thalamus and the basal ganglia (BG). The diffuse yet specific patterns of structural connectivity of the thalamus with the cortex suggest thalamocortical connectivity could play an important role in addressing the binding problem. Previous research has established the presence of BG oscillations and their link to functional and pathological connectivity states to the cortical structures. Considering the topographically organized connections between thalamus, BG and the cortex it has been proposed that disruptions to normal oscillatory activity within the cortico-BG-thalamocortical circuits may partly account for the pathophysiology of Parkinson's disease (PD) . Using simultaneous invasive recordings of cortical and thalamic electrophysiological activity in two awake and spontaneously behaving human subjects, we provide direct evidence of thalamic regulation of cortical activity through a mechanism of phase-amplitude coupling (PAC). Specifically, we show that cortical PAC between the θ phase and β amplitude is spatially dependent on and time variant with the magnitude of thalamocortical θ coherence. Moreover, using causality analysis and MR diffusion tractrography, we provide evidence that thalamic θ activity drives cortical θ oscillations and PAC across structures via structurally constrained pathways..In PD, pathologic oscillatory activity, particularly in the β band, is present in BG and motor cortex. The role of these β oscillations in modulating activity at a network level have not been thoroughly characterized. Using simultaneously recorded cortical and pallidal local field potentials in 20 patients with PD undergoing deep brain stimulation surgery, we confirm increased β activity and β-γ PAC in motor cortical areas. The cortical β band is highly coherent with β activity in the motor region of the GPi where local β-γ and β-(200-300Hz) PAC and cross-site pallido-cortical PAC were observed. Contralateral movement significantly decreased pallido-cortical coherence and PAC as well as local cortical PAC, but did not completely eliminate this coupling, possibly manifesting a deficiency in the diseased BG to disentrain the motor network during action. These results shed light on the dynamic nature of pallidocortical coupling, suggesting β oscillations reverberate through the motor network and modulate activity at a network level.