Regulation of Motor Representation by Phase–Amplitude Coupling in the Sensorimotor Cortex

Abstract

High-␥ amplitude (80 -150 Hz) represents motor information, such as movement types, on the sensorimotor cortex. In several cortical areas, high-␥ amplitudes are coupled with low-frequency phases, e.g., ␣ and (phase-amplitude coupling, PAC). However, such coupling has not been studied in the sensorimotor cortex; thus, its potential functional role has yet to be explored. We investigated PAC of high-␥ amplitude in the sensorimotor cortex during waiting for and the execution of movements using electrocorticographic (ECoG) recordings in humans. ECoG signals were recorded from the sensorimotor cortices of 4 epilepsy patients while they performed three different hand movements. A subset of electrodes showed high-␥ activity selective to movement type around the timing of motor execution, while the same electrodes showed nonselective high-␥ activity during the waiting period (Ͼ2 s before execution). Cross frequency coupling analysis revealed that the high-␥ amplitude during waiting was strongly coupled with the ␣ phase (10 -14 Hz) at the electrodes with movement-selective high-␥ amplitudes during execution. This coupling constituted the high-␥ amplitude peaking around the trough of the ␣ oscillation, and its strength and phase were not predictive of movement type. As the coupling attenuated toward the timing of motor execution, the high-␥ amplitude appeared to be released fromthe␣phasetobuildamotorrepresentationwithphase-independentactivity.OurresultssuggestthatPACmodulatesmotorrepresentation in the sensorimotor cortex by holding and releasing high-␥ activity in movement-selective cortical regions.

Exaggerated phase–amplitude coupling in the primary motor cortex in Parkinson disease

“…Cortical broadband-γ spectral power increases in specific brain areas during performance of motor, visual, language, or cognitive tasks, is correlated with augmentation of the blood-oxygen leveldependent signal measured on functional MRI (24), and is thought to reflect underlying asynchronous spiking activity (25,26). In the normal state, the modulation of broadband-γ activity by the phase of low-frequency rhythms is highly dynamic and taskand site-specific (13,14,23). Excessive M1 phase-amplitude coupling in PD may reflect a pathological state in which the cortex is restricted to a monotonous pattern of coupling, rendering it less able to respond dynamically to signals from other cortical regions, such as frontal executive areas involved in internally directed movement.…”

“…Because of the temporal restrictions of human intraoperative studies, we sampled only one brief time epoch (30 s) at limited spatial locations in the off-medication state only. Studies of interictal LFPs in humans with epilepsy recorded with larger 128-channels grids show that, normally, phase-amplitude coupling is present only in a small sample of recordings, and slight changes in behavioral state affect the location and timing of coupling (7,10,12,13). Here, we typically had only one contact covering M1 of movement disorder patients, and we recorded from only a single bipolar pair in STN.…”

Suppression of spontaneous oscillations in high-frequency stimulated neuron models

“…However, the low-frequency and the high-frequency oscillations interact under both physiological [56] and pathological [57] conditions. For instance, physiological processes in motor circuits may be perturbed by a coupling of the HFO amplitude [57,58] to the phase of beta oscillations.…”

A θ–γ Oscillation Code for Neuronal Coordination during Motor Behavior

“…The motor cortex of humans shows a transient increase in ␥ band (80 Hz) activity around the time of movement (Crone et al, 1998;Gaetz et al, 2010;Yanagisawa et al, 2012), as in the high-␥ activity reported here, whereas (8 -14 Hz) and ␤ (15-30 Hz) oscillations are prominent during movement preparation and suppressed during movement execution (Miller et al, 2012). Similar changes in ␤ power are also known in monkeys (Baker et al, 1997;Reimer and Hatsopoulos, 2010).…”