scholarly journals Modulation of dopamine tone induces frequency shifts in cortico-basal ganglia beta oscillations

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
L. Iskhakova ◽  
P. Rappel ◽  
M. Deffains ◽  
G. Fonar ◽  
O. Marmor ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Phase Locking ◽  
Oscillatory Activity ◽  
Dopamine Depletion ◽  
Beta Oscillations ◽  
Strongly Coupled ◽  
Beta Power ◽  
Oscillatory Power ◽  
Phase Amplitude ◽  
Beta Frequency

AbstractΒeta oscillatory activity (human: 13–35 Hz; primate: 8–24 Hz) is pervasive within the cortex and basal ganglia. Studies in Parkinson’s disease patients and animal models suggest that beta-power increases with dopamine depletion. However, the exact relationship between oscillatory power, frequency and dopamine tone remains unclear. We recorded neural activity in the cortex and basal ganglia of healthy non-human primates while acutely and chronically up- and down-modulating dopamine levels. We assessed changes in beta oscillations in patients with Parkinson’s following acute and chronic changes in dopamine tone. Here we show beta oscillation frequency is strongly coupled with dopamine tone in both monkeys and humans. Power, coherence between single-units and local field potentials (LFP), spike-LFP phase-locking, and phase-amplitude coupling are not systematically regulated by dopamine levels. These results demonstrate that beta frequency is a key property of pathological oscillations in cortical and basal ganglia networks.

scholarly journals Frequency matters: Up- and Down-Regulation of Dopamine Tone Induces Similar Frequency Shifts in Cortico-Basal Ganglia Beta Oscillations

2020 ◽  
Author(s):  
L. Iskhakova ◽  
P. Rappel ◽  
G. Fonar ◽  
O. Marmor ◽  
R. Paz ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Phase Locking ◽  
Oscillatory Activity ◽  
Dopamine Depletion ◽  
Beta Oscillations ◽  
Similar Frequency ◽  
Strongly Coupled ◽  
Beta Power ◽  
Oscillatory Power ◽  
Network Studies

AbstractBeta oscillatory activity (13-30Hz) is pervasive within the cortico-basal ganglia (CBG) network. Studies in Parkinson’s disease (PD) patients and animal models suggested that beta-power increases with dopamine depletion. However, the exact relationship between oscillatory power, frequency and dopamine-tone remains unclear. We recorded neural activity in the CBG network of non-human-primates (NHP) while acutely up- and down-modulating dopamine levels. Further, we assessed changes in beta oscillations of PD patients following acute and chronic changes in dopamine-tone. Beta oscillation frequency was strongly coupled with dopamine-tone in both NHPs and human patients. In contrast, power, coherence between single-units and LFP, and spike-LFP phase-locking were not systematically regulated by dopamine levels. These results demonstrate via causal manipulations that frequency, rather than other properties, is the key property of pathological oscillations in the CBG networks. These insights can lead to improvements in understanding of CBG physiology, PD progression tracking and patient care.

scholarly journals Aberrant striatal oscillations after dopamine loss in parkinsonian non-human primates

2019 ◽  
Author(s):  
Arun Singh ◽  
Stella M. Papa
Keyword(s):  
Basal Ganglia ◽  
Oscillatory Activity ◽  
Field Potentials ◽  
Striatal Neurons ◽  
Dopamine Depletion ◽  
Frequency Bands ◽  
Oscillatory Pattern ◽  
Motor Abnormalities ◽  
Beta Frequency

AbstractDopamine depletion in Parkinson’s disease (PD) is associated with abnormal oscillatory activity in the cortico-basal ganglia network. However, the oscillatory pattern of striatal neurons in PD remains poorly defined. Here, we analyzed the local field potentials in one untreated and five MPTP-treated non-human primates (NHP) to model advanced PD. Augmented oscillatory activity in the alpha (8-13 Hz) and low-beta (13-20 Hz) frequency bands was found in the striatum in parallel to the motor cortex and globus pallidus of the NHP-PD model. The coherence analysis showed increased connectivity in the cortico-striatal and striato-pallidal pathways at alpha and low-beta frequency bands, confirming the presence of abnormal 8-20 Hz activity in the cortico-basal ganglia network. The acute L-Dopa injection that induced a clear motor response normalized the amplified 8-20 Hz oscillations. These findings indicate that pathological striatal oscillations at alpha and low-beta bands are concordant with the basal ganglia network changes after dopamine depletion, and thereby support a key role of the striatum in the generation of parkinsonian motor abnormalities.

scholarly journals Dopamine depletion can be predicted by the aperiodic component of subthalamic local field potentials

2021 ◽  
Author(s):  
Jinmo Kim ◽  
Jungmin Lee ◽  
Eunho Kim ◽  
Joon Ho Choi ◽  
Jong-Cheol Rah ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Gamma Oscillations ◽  
Significant Negative Correlation ◽  
Field Potentials ◽  
Dopamine Depletion ◽  
Frequency Oscillation ◽  
Beta Power ◽  
Aperiodic Component ◽  
Beta Frequency ◽  
Nigrostriatal Lesion

Electrophysiological biomarkers reflecting the pathological activities in the basal ganglia are essential to gain an etiological understanding of Parkinson′s disease (PD) and develop a method of diagnosing and treating the disease. Previous studies that explored electrophysiological biomarkers in PD have focused mainly on oscillatory or periodic activities such as beta and gamma oscillations. Emerging evidence has suggested that the nonoscillatory, aperiodic component reflects the firing rate and synaptic current changes corresponding to cognitive and pathological states. Nevertheless, it has never been thoroughly examined whether the aperiodic component can be used as a biomarker that reflect pathological activities in the basal ganglia in PD. In this study, we examined the parameters of the aperiodic component and tested its practicality as an electrophysiological biomarker of pathological activity in PD. We found that a set of aperiodic parameters, aperiodic offset and exponent, were significantly decreased by the nigrostriatal lesion. To further prove the usefulness of the parameters as biomarkers, acute levodopa treatment reverted the aperiodic offset. We then compared the aperiodic parameters with a previously established periodic biomarker of PD, beta frequency oscillation. We found a moderately significant negative correlation with beta power. Finally, taking the aperiodic parameters into account, we could significantly improve the beta power-based prediction of pathological activities in the basal ganglia, demonstrating the validity of these parameters as biomarkers.

scholarly journals Beta band oscillations in motor cortex reflect neural population signals that delay movement onset

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Preeya Khanna ◽  
Jose M Carmena
Keyword(s):  
Motor Cortex ◽  
Neural Activity ◽  
Oscillatory Activity ◽  
Neural Population ◽  
Beta Band ◽  
Neural Basis ◽  
Movement Onset ◽  
Beta Oscillations ◽  
Beta Power ◽  
Oscillatory Power

Motor cortical beta oscillations have been reported for decades, yet their behavioral correlates remain unresolved. Some studies link beta oscillations to changes in underlying neural activity, but the specific behavioral manifestations of these reported changes remain elusive. To investigate how changes in population neural activity, beta oscillations, and behavior are linked, we recorded multi-scale neural activity from motor cortex while three macaques performed a novel neurofeedback task. Subjects volitionally brought their beta oscillatory power to an instructed state and subsequently executed an arm reach. Reaches preceded by a reduction in beta power exhibited significantly faster movement onset times than reaches preceded by an increase in beta power. Further, population neural activity was found to shift farther from a movement onset state during beta oscillations that were neurofeedback-induced or naturally occurring during reaching tasks. This finding establishes a population neural basis for slowed movement onset following periods of beta oscillatory activity.

scholarly journals Cross-frequency Phase–Amplitude Coupling as a Mechanism for Temporal Orienting of Attention in Childhood

2018 ◽  
Vol 30 (4) ◽  
pp. 594-602 ◽  
Author(s):  
Giovanni Mento ◽  
Duncan E. Astle ◽  
Gaia Scerif
Keyword(s):  
Inverse Correlation ◽  
Human Cognition ◽  
Response Preparation ◽  
Strongly Coupled ◽  
Oscillatory Dynamics ◽  
Beta Power ◽  
Temporal Intervals ◽  
Phase Amplitude ◽  
Frequency Phase ◽  
Temporal Orienting

Temporal orienting of attention operates by biasing the allocation of cognitive and motor resources in specific moments in time, resulting in the improved processing of information from expected compared with unexpected targets. Recent findings have shown that temporal orienting operates relatively early across development, suggesting that this attentional mechanism plays a core role for human cognition. However, the exact neurophysiological mechanisms allowing children to attune their attention over time are not well understood. In this study, we presented 8- to 12-year-old children with a temporal cueing task designed to test (1) whether anticipatory oscillatory dynamics predict children's behavioral performance on a trial-by-trial basis and (2) whether anticipatory oscillatory neural activity may be supported by cross-frequency phase–amplitude coupling as previously shown in adults. Crucially, we found that, similar to what has been reported in adults, children's ongoing beta rhythm was strongly coupled with their theta rhythm and that the strength of this coupling distinguished validly cued temporal intervals, relative to neutral cued trials. In addition, in long trials, there was an inverse correlation between oscillatory beta power and children's trial-by-trial reaction, consistent with oscillatory beta power reflecting better response preparation. These findings provide the first experimental evidence that temporal attention in children operates by exploiting oscillatory mechanism.

scholarly journals Temporal evolution of beta bursts in the parkinsonian cortical and basal ganglia network

2019 ◽  
Vol 116 (32) ◽  
pp. 16095-16104 ◽  
Author(s):  
Hayriye Cagnan ◽  
Nicolas Mallet ◽  
Christian K. E. Moll ◽  
Alessandro Gulberti ◽  
Abbey B. Holt ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Temporal Evolution ◽  
Phase Locking ◽  
Stable Phase ◽  
Striatal Neurons ◽  
Action Potential Firing ◽  
Beta Oscillations ◽  
Oscillation Phase ◽  
Potential Firing ◽  
Basal Ganglia Structures

Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around the emergence of cortical beta bursts (β bursts), transient (50 to 350 ms) increases in the beta amplitude of cortical signals. In PD patients, the phase locking of background spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset and followed the temporal profile of cortical β bursts, with conditions of synchronization consistent within and across bursts. Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum. The onset of consistent phase-locking conditions was preceded by abrupt phase slips between cortical and basal ganglia ensemble signals. Single-unit recordings demonstrated that ensemble-level properties of synchronization were not underlain by changes in firing rate but, rather, by the timing of action potentials in relation to cortical oscillation phase. Notably, the preferred angle of phase-locked action potential firing in each basal ganglia structure was shifted during burst initiation, then maintained stable phase relations during the burst. Subthalamic, pallidal, and striatal neurons engaged and disengaged with cortical β bursts to different extents and timings. The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, which could be key for the generation/ maintenance of excessive beta oscillations in parkinsonism.

Brain Networks Related to Beta Oscillatory Activity during Episodic Memory Retrieval

2018 ◽  
Vol 30 (2) ◽  
pp. 174-187 ◽  
Author(s):  
Erika Nyhus
Keyword(s):  
Frontal Cortex ◽  
Oscillatory Activity ◽  
Episodic Retrieval ◽  
Beta Oscillations ◽  
New Words ◽  
Memory Suppression ◽  
Frontoparietal Network ◽  
Beta Power ◽  
Place Task ◽  
The Right

Evidence from fMRI has consistently located a widespread network of frontal, parietal, and temporal lobe regions during episodic retrieval. However, the temporal limitations of the fMRI methodology have made it difficult to assess the transient network dynamics by which these distributed regions coordinate activity. Recent evidence suggests that beta oscillations (17–20 Hz) are important for top–down control for memory suppression. However, the spatial limitations of the EEG methodology make it difficult to assess the relationship between these oscillatory signals and the distributed networks identified with fMRI. This study used simultaneous EEG/fMRI to identify networks related to beta oscillations during episodic retrieval. Participants studied adjectives and either imagined a scene (Place Task) or judged its pleasantness (Pleasant Task). During the recognition test, participants decided which task was performed with each word (“Old Place Task” or “Old Pleasant Task”) or “New.” EEG results revealed that posterior beta power was greater for new than old words. fMRI results revealed activity in a frontal, parietal network that was greater for old than new words, consistent with prior studies. Although overall beta power increases correlated with decreased activity within a predominantly parietal network, within the right dorsolateral and ventrolateral pFC, beta power correlated with BOLD activity more under conditions requiring more cognitive control and EEG/fMRI effects in the right frontal cortex correlated with BOLD activity in a frontoparietal network. Therefore, using simultaneous EEG and fMRI, the present results suggest that beta oscillations are related to postretrieval control operations in the right frontal cortex and act within a broader postretrieval control network.

scholarly journals Nonsinusoidal oscillations underlie pathological phase-amplitude coupling in the motor cortex in Parkinson’s disease

2016 ◽  
Author(s):  
Scott R. Cole ◽  
Erik J. Peterson ◽  
Roemer van der Meij ◽  
Coralie de Hemptinne ◽  
Philip A. Starr ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Motor Cortex ◽  
Field Potential ◽  
Synaptic Activity ◽  
Motor Deficit ◽  
Beta Oscillations ◽  
High Gamma ◽  
Phase Amplitude

AbstractParkinson’s disease (PD) is associated with abnormal beta oscillations (13-30 Hz) in the basal ganglia and motor cortex (M1). Recent reports show that M1 beta-high gamma (50-200 Hz) phase-amplitude coupling (PAC) is exaggerated in PD and is reduced following acute deep brain stimulation (DBS). Here we analyze invasive M1 electrocorticography recordings in PD patients on and off DBS, and in isolated cervical dystonia patients, and show that M1 beta oscillations are nonsinusoidal, having sharp and asymmetric features. These sharp oscillatory beta features underlie the previously reported PAC, providing an alternative to the standard interpretation of PAC as an interaction between two distinct frequency components. Specifically, the ratio between peak and trough sharpness is nearly perfectly correlated with beta-high gamma PAC (r = 0.96) and predicts PD-related motor deficit. Using a simulation of the local field potential, we demonstrate that sharp oscillatory waves can arise from synchronous synaptic activity. We propose that exaggerated beta-high gamma PAC may actually reflect such synchronous synaptic activity, manifesting as sharp beta oscillations that are “smoothed out” with DBS. These results support the “desynchronization” hypothesis of DBS wherein DBS counteracts pathological synchronization throughout the basal ganglia-thalamocortical loop. We argue that PAC can be influenced by more than one mechanism. In this case synaptic synchrony, rather than the often assumed spike-field coherence, may underlie exaggerated PAC. These often overlooked temporal features of the oscillatory waveform carry critical physiological information about neural processes and dynamics that may lead to better understanding of underlying neuropathology.

scholarly journals Input zone-selective dysrhythmia in motor thalamus after dopamine depletion

2021 ◽  
Author(s):  
Kouichi C. Nakamura ◽  
Andrew Sharott ◽  
Takuma Tanaka ◽  
Peter J. Magill
Keyword(s):  
Basal Ganglia ◽  
Slow Wave ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Brain State ◽  
Dependent Manner ◽  
Dopamine Depletion ◽  
Beta Band ◽  
Beta Oscillations ◽  
Motor Thalamus

AbstractThe cerebral cortex, basal ganglia and motor thalamus form circuits important for purposeful movement. In Parkinsonism, basal ganglia neurons often exhibit dysrhythmic activity during, and with respect to, the slow (∼1 Hz) and beta-band (15–30 Hz) oscillations that emerge in cortex in a brain state-dependent manner. There remains, however, a pressing need to elucidate the extent to which motor thalamus activity becomes similarly dysrhythmic after dopamine depletion relevant to Parkinsonism. To address this, we recorded single-neuron and ensemble outputs in the ‘basal ganglia-recipient zone’ (BZ) and ‘cerebellar-recipient zone’ (CZ) of motor thalamus in anesthetized male dopamine-intact rats and 6-OHDA-lesioned rats during two brain states, respectively defined by cortical slow-wave activity and activation. Two forms of thalamic input zone-selective dysrhythmia manifested after dopamine depletion: First, BZ neurons, but not CZ neurons, exhibited abnormal phase-shifted firing with respect to cortical slow oscillations prevalent during slow-wave activity; secondly, BZ neurons, but not CZ neurons, inappropriately synchronized their firing and engaged with the exaggerated cortical beta oscillations arising in activated states. These dysrhythmias were not accompanied by the thalamic hypoactivity predicted by canonical firing rate-based models of circuit organization in Parkinsonism. Complementary recordings of neurons in substantia nigra pars reticulata suggested their altered activity dynamics could underpin the BZ dysrhythmias. Finally, pharmacological perturbations demonstrated that ongoing activity in the motor thalamus bolsters exaggerated beta oscillations in motor cortex. We conclude that BZ neurons are selectively primed to mediate the detrimental influences of abnormal slow and beta-band rhythms on circuit information processing in Parkinsonism.

scholarly journals Abnormal beta power is a hallmark of explicit movement control in functional movement disorders

Neurology ◽  
2017 ◽  
Vol 90 (3) ◽  
pp. e247-e253 ◽  
Author(s):  
Tiago Teodoro ◽  
Anne Marthe Meppelink ◽  
Simon Little ◽  
Robert Grant ◽  
Glenn Nielsen ◽  
...  
Keyword(s):  
Movement Disorders ◽  
Movement Control ◽  
Motor Preparation ◽  
Functional Movement ◽  
Cue Validity ◽  
Cortical Oscillations ◽  
Beta Power ◽  
Oscillatory Power ◽  
Functional Movement Disorders ◽  
Beta Frequency

ObjectiveTo determine whether sensorimotor beta-frequency oscillatory power is raised during motor preparation in patients with functional movement disorders (FMD) and could therefore be a marker of abnormal “body-focused” attention.MethodsWe analyzed motor performance and beta-frequency cortical oscillations during a precued choice reaction time (RT) task with varying cue validity (50% or 95% congruence between preparation and go cues). We compared 21 patients with FMD with 13 healthy controls (HCs).ResultsIn HCs, highly predictive cues were associated with faster RT and beta desynchronization in the contralateral hemisphere (contralateral slope −0.045 [95% confidence interval (CI) −0.057 to −0.033] vs ipsilateral −0.033 [95% CI −0.046 to −0.021], p < 0.001) and with a tendency for reaching lower contralateral end-of-preparation beta power (contralateral −0.482 [95% CI −0.827 to −0.137] vs ipsilateral −0.328 [95% CI −0.673 to 0.016], p = 0.069). In contrast, patients with FMD had no improvement in RTs with highly predictive cues and showed an impairment of beta desynchronization and lateralization before movement.ConclusionsPersistent beta synchronization during motor preparation could reflect abnormal explicit control of movement in FMD. Excessive attention to movement itself rather than the goal might maintain beta synchronization and impair performance.

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