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• W2042420303 abstract "Beta oscillations in cortical-basal ganglia (BG) circuits have been implicated in normal movement suppression and motor impairment in Parkinson's disease. To dissect the functional correlates of these rhythms we compared neural activity during four distinct variants of a cued choice task in rats. Brief beta (∼20 Hz) oscillations occurred simultaneously throughout the cortical-BG network, both spontaneously and at precise moments of task performance. Beta phase was rapidly reset in response to salient cues, yet increases in beta power were not rigidly linked to cues, movements, or movement suppression. Rather, beta power was enhanced after cues were used to determine motor output. We suggest that beta oscillations reflect a postdecision stabilized state of cortical-BG networks, which normally reduces interference from alternative potential actions. The abnormally strong beta seen in Parkinson's Disease may reflect overstabilization of these networks, producing pathological persistence of the current motor state. Beta oscillations in cortical-basal ganglia (BG) circuits have been implicated in normal movement suppression and motor impairment in Parkinson's disease. To dissect the functional correlates of these rhythms we compared neural activity during four distinct variants of a cued choice task in rats. Brief beta (∼20 Hz) oscillations occurred simultaneously throughout the cortical-BG network, both spontaneously and at precise moments of task performance. Beta phase was rapidly reset in response to salient cues, yet increases in beta power were not rigidly linked to cues, movements, or movement suppression. Rather, beta power was enhanced after cues were used to determine motor output. We suggest that beta oscillations reflect a postdecision stabilized state of cortical-BG networks, which normally reduces interference from alternative potential actions. The abnormally strong beta seen in Parkinson's Disease may reflect overstabilization of these networks, producing pathological persistence of the current motor state. Transient beta rhythms naturally synchronize activity throughout the basal ganglia Beta oscillations are not rigidly coupled to sensory processing or motor output Rather, beta occurs once cues are used to determine a motor plan The elevated beta state may stabilize this plan against competing alternatives Strong beta-band (∼15–30 Hz) local field potential (LFP) oscillations are found in the BG and cortex of both humans with Parkinson's disease (PD; Weinberger et al., 2009Weinberger M. Hutchison W.D. Dostrovsky J.O. Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?.Exp. Neurol. 2009; 219: 58-61Crossref PubMed Scopus (90) Google Scholar, Levy et al., 2002Levy R. Ashby P. Hutchison W.D. Lang A.E. Lozano A.M. Dostrovsky J.O. Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.Brain. 2002; 125: 1196-1209Crossref PubMed Scopus (526) Google Scholar, Hammond et al., 2007Hammond C. Bergman H. Brown P. Pathological synchronization in Parkinson's disease: networks, models and treatments.Trends Neurosci. 2007; 30: 357-364Abstract Full Text Full Text PDF PubMed Scopus (1122) Google Scholar, Brown et al., 2001Brown P. Oliviero A. Mazzone P. Insola A. Tonali P. Di Lazzaro V. Dopamine dependency of oscillations between subthalamic nucleus and pallidum in Parkinson's disease.J. Neurosci. 2001; 21: 1033-1038PubMed Google Scholar) and dopamine-lesioned animals (Mallet et al., 2008bMallet N. Pogosyan A. Sharott A. Csicsvari J. Bolam J.P. Brown P. Magill P.J. Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex.J. Neurosci. 2008; 28: 4795-4806Crossref PubMed Scopus (316) Google Scholar, Sharott et al., 2005Sharott A. Magill P.J. Harnack D. Kupsch A. Meissner W. Brown P. Dopamine depletion increases the power and coherence of beta-oscillations in the cerebral cortex and subthalamic nucleus of the awake rat.Eur. J. Neurosci. 2005; 21: 1413-1422Crossref PubMed Scopus (280) Google Scholar). Beta power is reduced by treatments that improve bradykinesia and rigidity, including dopamine replacement therapy (Levy et al., 2002Levy R. Ashby P. Hutchison W.D. Lang A.E. Lozano A.M. Dostrovsky J.O. Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.Brain. 2002; 125: 1196-1209Crossref PubMed Scopus (526) Google Scholar, Brown et al., 2001Brown P. Oliviero A. Mazzone P. Insola A. Tonali P. Di Lazzaro V. Dopamine dependency of oscillations between subthalamic nucleus and pallidum in Parkinson's disease.J. Neurosci. 2001; 21: 1033-1038PubMed Google Scholar) and deep brain stimulation (Kühn et al., 2008Kühn A.A. Kempf F. Brücke C. Gaynor Doyle L. Martinez-Torres I. Pogosyan A. Trottenberg T. Kupsch A. Schneider G.H. Hariz M.I. et al.High-frequency stimulation of the subthalamic nucleus suppresses oscillatory beta activity in patients with Parkinson's disease in parallel with improvement in motor performance.J. Neurosci. 2008; 28: 6165-6173Crossref PubMed Scopus (567) Google Scholar, Wingeier et al., 2006Wingeier B. Tcheng T. Koop M.M. Hill B.C. Heit G. Bronte-Stewart H.M. Intra-operative STN DBS attenuates the prominent beta rhythm in the STN in Parkinson's disease.Exp. Neurol. 2006; 197: 244-251Crossref PubMed Scopus (195) Google Scholar). Conversely, artificially driving the subthalamic nucleus or motor cortex at beta frequencies slows movement (Chen et al., 2007Chen C.C. Litvak V. Gilbertson T. Kühn A. Lu C.S. Lee S.T. Tsai C.H. Tisch S. Limousin P. Hariz M. Brown P. Excessive synchronization of basal ganglia neurons at 20 Hz slows movement in Parkinson's disease.Exp. Neurol. 2007; 205: 214-221Crossref PubMed Scopus (174) Google Scholar, Pogosyan et al., 2009Pogosyan A. Gaynor L.D. Eusebio A. Brown P. Boosting cortical activity at Beta-band frequencies slows movement in humans.Curr. Biol. 2009; 19: 1637-1641Abstract Full Text Full Text PDF PubMed Scopus (428) Google Scholar). From these observations it has been hypothesized that beta oscillations in cortical-BG circuits are central to the systems-level pathophysiology of PD (Hammond et al., 2007Hammond C. Bergman H. Brown P. Pathological synchronization in Parkinson's disease: networks, models and treatments.Trends Neurosci. 2007; 30: 357-364Abstract Full Text Full Text PDF PubMed Scopus (1122) Google Scholar, Weinberger et al., 2009Weinberger M. Hutchison W.D. Dostrovsky J.O. Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?.Exp. Neurol. 2009; 219: 58-61Crossref PubMed Scopus (90) Google Scholar), perhaps by interfering with the highly decorrelated patterns of neuronal spiking proposed to characterize normal BG information processing (Nini et al., 1995Nini A. Feingold A. Slovin H. Bergman H. Neurons in the globus pallidus do not show correlated activity in the normal monkey, but phase-locked oscillations appear in the MPTP model of parkinsonism.J. Neurophysiol. 1995; 74: 1800-1805PubMed Google Scholar). However, beta oscillations are also observed in multiple brain regions of awake, healthy subjects, including the sensorimotor neocortex of nonhuman primates (Murthy and Fetz, 1992Murthy V.N. Fetz E.E. Coherent 25- to 35-Hz oscillations in the sensorimotor cortex of awake behaving monkeys.Proc. Natl. Acad. Sci. USA. 1992; 89: 5670-5674Crossref PubMed Scopus (759) Google Scholar, Sanes and Donoghue, 1993Sanes J.N. Donoghue J.P. Oscillations in local field potentials of the primate motor cortex during voluntary movement.Proc. Natl. Acad. Sci. USA. 1993; 90: 4470-4474Crossref PubMed Scopus (459) Google Scholar), mouse hippocampus (Berke et al., 2008Berke J.D. Hetrick V. Breck J. Greene R.W. Transient 23-30 Hz oscillations in mouse hippocampus during exploration of novel environments.Hippocampus. 2008; 18: 519-529Crossref PubMed Scopus (75) Google Scholar), rat olfactory circuits (Kay et al., 2009Kay L.M. Beshel J. Brea J. Martin C. Rojas-Líbano D. Kopell N. Olfactory oscillations: the what, how and what for.Trends Neurosci. 2009; 32: 207-214Abstract Full Text Full Text PDF PubMed Scopus (214) Google Scholar), and the striatum in rats (Berke et al., 2004Berke J.D. Okatan M. Skurski J. Eichenbaum H.B. Oscillatory entrainment of striatal neurons in freely moving rats.Neuron. 2004; 43: 883-896Abstract Full Text Full Text PDF PubMed Scopus (365) Google Scholar), nonhuman primates (Courtemanche et al., 2003Courtemanche R. Fujii N. Graybiel A.M. Synchronous, focally modulated beta-band oscillations characterize local field potential activity in the striatum of awake behaving monkeys.J. Neurosci. 2003; 23: 11741-11752PubMed Google Scholar), and humans (Sochurkova and Rektor, 2003Sochurkova D. Rektor I. Event-related desynchronization/synchronization in the putamen. An SEEG case study.Exp. Brain Res. 2003; 149: 401-404PubMed Google Scholar). Cortical beta power is elevated during maintenance of a static position (Baker et al., 1997Baker S.N. Olivier E. Lemon R.N. Coherent oscillations in monkey motor cortex and hand muscle EMG show task-dependent modulation.J. Physiol. 1997; 501: 225-241Crossref PubMed Scopus (501) Google Scholar), active suppression of movement initiation (Swann et al., 2009Swann N. Tandon N. Canolty R. Ellmore T.M. McEvoy L.K. Dreyer S. DiSano M. Aron A.R. Intracranial EEG reveals a time- and frequency-specific role for the right inferior frontal gyrus and primary motor cortex in stopping initiated responses.J. Neurosci. 2009; 29: 12675-12685Crossref PubMed Scopus (326) Google Scholar), and postmovement hold periods (Pfurtscheller et al., 1996Pfurtscheller G. Stancák Jr., A. Neuper C. Post-movement beta synchronization. A correlate of an idling motor area?.Electroencephalogr. Clin. Neurophysiol. 1996; 98: 281-293Abstract Full Text PDF PubMed Scopus (506) Google Scholar). Conversely, cortical beta power has been observed to decrease during movement preparation and initiation (Pfurtscheller et al., 2003Pfurtscheller G. Graimann B. Huggins J.E. Levine S.P. Schuh L.A. Spatiotemporal patterns of beta desynchronization and gamma synchronization in corticographic data during self-paced movement.Clin. Neurophysiol. 2003; 114: 1226-1236Abstract Full Text Full Text PDF PubMed Scopus (327) Google Scholar, Zhang et al., 2008Zhang Y. Chen Y. Bressler S.L. Ding M. Response preparation and inhibition: the role of the cortical sensorimotor beta rhythm.Neuroscience. 2008; 156: 238-246Crossref PubMed Scopus (204) Google Scholar). These results have been taken as evidence that beta oscillations reflect “maintenance of the status quo” in the motor system (Engel and Fries, 2010Engel A.K. Fries P. Beta-band oscillations—signalling the status quo?.Curr. Opin. Neurobiol. 2010; 20: 156-165Crossref PubMed Scopus (1560) Google Scholar). This concept fits well with the proposed pathophysiological role of beta oscillations in PD, where patients have difficulty not only initiating movement, but also in stopping or switching between motor programs (Stoffers et al., 2001Stoffers D. Berendse H.W. Deijen J.B. Wolters E.C. Motor perseveration is an early sign of Parkinson's disease.Neurology. 2001; 57: 2111-2113Crossref PubMed Scopus (39) Google Scholar). However, studies of beta oscillations within BG circuits have usually involved subjects that were anesthetized, dopamine-depleted, or not engaged in specific behaviors, so the natural correlates of BG beta oscillations are not well defined. Here we investigate the functional correlates of BG beta oscillations in intact, unrestrained rats. We recorded simultaneously from multiple structures to assess whether beta rhythms coordinate activity throughout the BG network. The rats performed four task variants that make different demands for behavioral control: subjects were instructed to promptly make specific movements (“Immediate-GO”), program movements but delay their execution (“Deferred-GO”), inhibit movements (“NOGO”), or cancel movements-in-preparation (“STOP”). By comparing beta power time courses under each condition, we examined how dynamic states of cortical-BG circuits relate to distinct sensorimotor subprocesses. We first examined LFPs recorded from the striatum (STR), globus pallidus (GP), and primary motor cortex (M1) during a choice reaction time task. Rats initiated trials by poking and holding their position within an illuminated nose-port (Figures 1A and 1B ). After a variable interval, one of two instruction cues (1 kHz, 4 kHz tones) directed the rat to quickly move his nose one port to the left or right, respectively. We have previously shown that contralateral performance in this “Immediate-GO” task is dependent on intact function of sensorimotor striatum (Gage et al., 2010Gage G.J. Stoetzner C.R. Wiltschko A.B. Berke J.D. Selective activation of striatal fast-spiking interneurons during choice execution.Neuron. 2010; 67: 466-479Abstract Full Text Full Text PDF PubMed Scopus (179) Google Scholar). Beta oscillations (15–25 Hz) were consistently more pronounced in STR and GP compared to M1, yet in each structure beta power was similarly modulated by task events (Figure 1C). Beta power initially dipped as rats entered the first port and stayed there (Nose In). This was followed by a sharp beta increase (“event-related synchronization,” ERS) after the instruction tone (Cue/Go), which peaked just after they initiated their chosen movement (Nose Out). There was a further abrupt decrease in beta power (an “event-related desynchronization,” ERD) as rats completed this movement (Side In), which triggered an audible food pellet delivery click on correct trials. Movement initiation is typically associated with beta ERDs, in contrast to the ERS that we observed. However, most prior studies have either used self-paced movements (Pfurtscheller et al., 2003Pfurtscheller G. Graimann B. Huggins J.E. Levine S.P. Schuh L.A. Spatiotemporal patterns of beta desynchronization and gamma synchronization in corticographic data during self-paced movement.Clin. Neurophysiol. 2003; 114: 1226-1236Abstract Full Text Full Text PDF PubMed Scopus (327) Google Scholar, Alegre et al., 2005Alegre M. Alonso-Frech F. Rodríguez-Oroz M.C. Guridi J. Zamarbide I. Valencia M. Manrique M. Obeso J.A. Artieda J. Movement-related changes in oscillatory activity in the human subthalamic nucleus: ipsilateral vs. contralateral movements.Eur. J. Neurosci. 2005; 22: 2315-2324Crossref PubMed Scopus (137) Google Scholar) or imposed a delay between instruction cues and the corresponding movements (MacKay and Mendonça, 1995MacKay W.A. Mendonça A.J. Field potential oscillatory bursts in parietal cortex before and during reach.Brain Res. 1995; 704: 167-174Crossref PubMed Scopus (66) Google Scholar, Baker et al., 1997Baker S.N. Olivier E. Lemon R.N. Coherent oscillations in monkey motor cortex and hand muscle EMG show task-dependent modulation.J. Physiol. 1997; 501: 225-241Crossref PubMed Scopus (501) Google Scholar, Rubino et al., 2006Rubino D. Robbins K.A. Hatsopoulos N.G. Propagating waves mediate information transfer in the motor cortex.Nat. Neurosci. 2006; 9: 1549-1557Crossref PubMed Scopus (308) Google Scholar, Sanes and Donoghue, 1993Sanes J.N. Donoghue J.P. Oscillations in local field potentials of the primate motor cortex during voluntary movement.Proc. Natl. Acad. Sci. USA. 1993; 90: 4470-4474Crossref PubMed Scopus (459) Google Scholar, Kühn et al., 2004Kühn A.A. Williams D. Kupsch A. Limousin P. Hariz M. Schneider G.H. Yarrow K. Brown P. Event-related beta desynchronization in human subthalamic nucleus correlates with motor performance.Brain. 2004; 127: 735-746Crossref PubMed Scopus (519) Google Scholar). We therefore examined beta power during a second task version (“Deferred-GO,” Figure 1B). In this task, subjects can use the instruction cue to prepare a movement, but to obtain reward they must delay execution until presentation of a separate “Go” signal. Information about the behavior of each rat in each task is given in Table S1 (available online). Rats trained in the Immediate-GO and Deferred-GO tasks attempted similar numbers of trials per session (averaging 173 and 160, respectively), consistent with similar levels of motivation. In the Deferred-GO task the patterns of beta power (Figure 1D) more closely matched prior studies of nonhuman primate sensorimotor cortex (Sanes and Donoghue, 1993Sanes J.N. Donoghue J.P. Oscillations in local field potentials of the primate motor cortex during voluntary movement.Proc. Natl. Acad. Sci. USA. 1993; 90: 4470-4474Crossref PubMed Scopus (459) Google Scholar, MacKay and Mendonça, 1995MacKay W.A. Mendonça A.J. Field potential oscillatory bursts in parietal cortex before and during reach.Brain Res. 1995; 704: 167-174Crossref PubMed Scopus (66) Google Scholar, Rubino et al., 2006Rubino D. Robbins K.A. Hatsopoulos N.G. Propagating waves mediate information transfer in the motor cortex.Nat. Neurosci. 2006; 9: 1549-1557Crossref PubMed Scopus (308) Google Scholar, Baker et al., 1997Baker S.N. Olivier E. Lemon R.N. Coherent oscillations in monkey motor cortex and hand muscle EMG show task-dependent modulation.J. Physiol. 1997; 501: 225-241Crossref PubMed Scopus (501) Google Scholar) and human subthalamic nucleus (Williams et al., 2003Williams D. Kühn A. Kupsch A. Tijssen M. van Bruggen G. Speelman H. Hotton G. Yarrow K. Brown P. Behavioural cues are associated with modulations of synchronous oscillations in the human subthalamic nucleus.Brain. 2003; 126: 1975-1985Crossref PubMed Scopus (93) Google Scholar). For both tasks we observed a beta ERS several hundred milliseconds after instruction cue onset, even though the behaviors occurring at this time were very different (moving for Immediate-GO, holding for Deferred-GO). Conversely, some key epochs with similar overt behavior between tasks were associated with very different levels of beta power. This is most obvious around the time of Go cues (third panel of Figure 1D), for which rats in both tasks were maintaining a hold in the initial nose-port during epoch “1,” and initiating movement during epoch “2.” Providing advance information about movement direction affects reaction times (RTs) (Luce, 1986Luce R.D. Response Times: Their Role in Inferring Elementary Mental Organization. Oxford University Press, New York, NY1986Google Scholar). We examined individual RT distributions (Figures S1C and S1D) to assess their contribution to beta power differences between tasks. Rats performing the Deferred-GO task had bimodal RT distributions consistent with their sometimes reacting to the Go cue, but sometimes anticipating it (Gage et al., 2010Gage G.J. Stoetzner C.R. Wiltschko A.B. Berke J.D. Selective activation of striatal fast-spiking interneurons during choice execution.Neuron. 2010; 67: 466-479Abstract Full Text Full Text PDF PubMed Scopus (179) Google Scholar). Strikingly, there was a beta ERS after the Go cue only for long-RT (>300 ms; presumed reactive) trials. On short-RT (<300 ms; presumed anticipatory) trials we found a beta ERD instead. During the Immediate-GO task, for which the rats do not know which way to go until the Cue/Go event, the beta ERS was observed for both long- and short-RT trials. From the Immediate- and Deferred-GO tasks, we draw several interim conclusions. First, beta power increases are not simply associated with holding position during delay periods, since in neither task did we see increased beta as subjects waited for the instruction cue. Second, beta power increases are not simply associated with movement, since the instruction cue produced a very similar beta ERS regardless of whether the instructed movement was performed immediately or was deferred. Third, presentation of a salient, task-relevant cue is not sufficient, since the beta ERS only followed the Go cue when the rats reacted to this cue, rather than having already anticipated it. Also inconsistent with a purely sensory response is the tighter locking of the beta ERS to movement onset than to the cue on Immediate-GO trials (Figure 1D). To further investigate the functional correlates of BG beta oscillations, another group of rats was tested during two additional task variants (“Go/NoGo,” “Stop-Signal”). These closely resembled the Immediate-Go task but incorporated cued movement suppression on some trials. To assess the organization of beta oscillations within the BG, implants targeted STR, GP, subthalamic nucleus (STN), and substantia nigra pars reticulata (SNr; Figures 2A and Figures S3A), together with a frontal electrocorticogram (ECoG). We found that beta oscillations occur simultaneously throughout the BG network (Figure 2B), in ∼100–200 ms epochs (Figure S2A) that involve the cortical site as well. In plots of power spectral density (Figure 2C), each rat had peak BG beta frequency slightly below 20 Hz (range: 17.9–19.5 Hz) with cortical frequency consistently a touch higher (18.4 Hz to 20.4 Hz). If beta oscillations represent a distinct, network-wide coordinated BG state, this should be apparent in analyses of phase and power relationships between structures. Coherence between all BG structures consistently showed a peak at ∼20 Hz for all rats (Figures 2D and Figures S3B). By contrast, we have previously shown that coherence between striatum and dorsal hippocampus in behaving rats is close to zero at 20 Hz (Berke et al., 2004Berke J.D. Okatan M. Skurski J. Eichenbaum H.B. Oscillatory entrainment of striatal neurons in freely moving rats.Neuron. 2004; 43: 883-896Abstract Full Text Full Text PDF PubMed Scopus (365) Google Scholar, Berke, 2009Berke J.D. Fast oscillations in cortical-striatal networks switch frequency following rewarding events and stimulant drugs.Eur. J. Neurosci. 2009; 30: 848-859Crossref PubMed Scopus (163) Google Scholar). We next constructed comodulograms, which illustrate the extent to which moment-to-moment oscillatory power covaries between structures (Buzsáki et al., 2003Buzsáki G. Buhl D.L. Harris K.D. Csicsvari J. Czéh B. Morozov A. Hippocampal network patterns of activity in the mouse.Neuroscience. 2003; 116: 201-211Crossref PubMed Scopus (339) Google Scholar). Coordinated power changes within the BG network were observed especially at ∼20 Hz (Figures 2D and Figures S3B). Modulation of beta power relative to behavioral events was essentially identical throughout the BG, and similar between BG and ECoG (Figure S2B). There was no consistent difference in the modulation of beta power for ipsilateral versus contralateral movements (Figure S4). We have previously reported that striatal LFPs show mutually exclusive dynamic states, characterized by combinations of either ∼20 Hz beta and ∼50 Hz low-gamma rhythms, or ∼8 Hz theta and ∼80 Hz high-gamma rhythms, respectively (Berke, 2009Berke J.D. Fast oscillations in cortical-striatal networks switch frequency following rewarding events and stimulant drugs.Eur. J. Neurosci. 2009; 30: 848-859Crossref PubMed Scopus (163) Google Scholar; see also Dejean et al., 2011Dejean C. Arbuthnott G. Wickens J.R. Le Moine C. Boraud T. Hyland B.I. Power fluctuations in beta and gamma frequencies in rat globus pallidus: association with specific phases of slow oscillations and differential modulation by dopamine D1 and D2 receptors.J. Neurosci. 2011; 31: 6098-6107Crossref PubMed Scopus (27) Google Scholar). These distinct states were visible in our current comodulograms: in STR, GP, and STN ∼50 Hz power was positively correlated with beta power and negatively correlated with ∼80 Hz activity. These relationships were absent or diminished for SNr. BG beta rhythms were tightly coordinated between structures, but not identical in all respects. We consistently observed a significant difference in beta phase between simultaneously recorded subregions (28 pairwise comparisons, p < 0.05 in every case; see Experimental Procedures). Although the specific set of recording regions varied between subjects, for all four rats we were able to compare beta phases between frontal ECoG, STR, and GP (Figure 2E). STR beta was always phase-advanced relative to the ECoG, (by an average of 97°), and GP was always slightly phase-advanced relative to the striatum (by an average of 4.8°). These results rule out some nonphysiological explanations for coordinated beta rhythms throughout the BG—for example, if the beta oscillations were on the common reference electrode, they would show no phase shift across regions. However, phase differences do not necessarily indicate where an ERS/ERD occurs first, especially as beta has a different phase at the cortical surface compared to deep layers (Murthy and Fetz, 1992Murthy V.N. Fetz E.E. Coherent 25- to 35-Hz oscillations in the sensorimotor cortex of awake behaving monkeys.Proc. Natl. Acad. Sci. USA. 1992; 89: 5670-5674Crossref PubMed Scopus (759) Google Scholar). We therefore also examined the slopes of the phase spectra between the ECoG, STR, and GP at beta frequencies (Figure S3C), which provides a measure of signal delay (Brown et al., 1998Brown P. Salenius S. Rothwell J.C. Hari R. Cortical correlate of the Piper rhythm in humans.J. Neurophysiol. 1998; 80: 2911-2917PubMed Google Scholar). The consistently very shallow slopes indicate that beta oscillations emerge with only small time delays throughout the cortical-BG network. Overall, our results are consistent with ∼20 Hz beta having a selective, distinct role in coordinating information processing within the BG of normal behaving animals. To explore beta timing in more detail, we examined trial-by-trial LFP traces during GO trials (Figure 3A ). Epochs of high beta power appeared to occur stochastically, with some task events either increasing (Cue) or diminishing (Side In) the probability of entering this beta state. Around detected movement onset (Nose Out) the pattern of beta power change was unexpectedly complex, showing a marked dependence on reaction time. For the most rapid responses, the beta ERS began around the time of movement onset and peaked shortly afterwards (Figures 3A and 3B). On trials with slower responses, the beta ERS began well before movements and was mostly completed by movement onset. To quantify this phenomenon we compared beta power for fast- versus slow-RT trials during the 300 ms epochs immediately preceding and following movement onset (Figure 3B, top). In both epochs all subjects had a significant difference in beta power (paired t tests before Nose out: for 3 rats p < 10−4, for the other p = 0.024; after Nose out: p < 10−3 for all rats). In addition, we calculated correlation coefficients between beta power and reaction time at each moment during task performance (Figure 3B, bottom). A strong positive correlation was found about 750 ms after the Cue event, driven by the ERD that is maximal around movement completion (see Kühn et al., 2004Kühn A.A. Williams D. Kupsch A. Limousin P. Hariz M. Schneider G.H. Yarrow K. Brown P. Event-related beta desynchronization in human subthalamic nucleus correlates with motor performance.Brain. 2004; 127: 735-746Crossref PubMed Scopus (519) Google Scholar, Williams et al., 2005Williams D. Kühn A. Kupsch A. Tijssen M. van Bruggen G. Speelman H. Hotton G. Loukas C. Brown P. The relationship between oscillatory activity and motor reaction time in the parkinsonian subthalamic nucleus.Eur. J. Neurosci. 2005; 21: 249-258Crossref PubMed Scopus (108) Google Scholar for related observations in humans). In addition, a smaller but reliable correlation occurred ∼30–100 ms before movement initiation. This suggests that the presence of the high-beta state during a critical period delays movement onset, consistent with evidence in humans associating increased beta power with slower movements (Levy et al., 2002Levy R. Ashby P. Hutchison W.D. Lang A.E. Lozano A.M. Dostrovsky J.O. Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease.Brain. 2002; 125: 1196-1209Crossref PubMed Scopus (526) Google Scholar, Brown et al., 2001Brown P. Oliviero A. Mazzone P. Insola A. Tonali P. Di Lazzaro V. Dopamine dependency of oscillations between subthalamic nucleus and pallidum in Parkinson's disease.J. Neurosci. 2001; 21: 1033-1038PubMed Google Scholar, Chen et al., 2007Chen C.C. Litvak V. Gilbertson T. Kühn A. Lu C.S. Lee S.T. Tsai C.H. Tisch S. Limousin P. Hariz M. Brown P. Excessive synchronization of basal ganglia neurons at 20 Hz slows movement in Parkinson's disease.Exp. Neurol. 2007; 205: 214-221Crossref PubMed Scopus (174) Google Scholar, Pogosyan et al., 2009Pogosyan A. Gaynor L.D. Eusebio A. Brown P. Boosting cortical activity at Beta-band frequencies slows movement in humans.Curr. Biol. 2009; 19: 1637-1641Abstract Full Text Full Text PDF PubMed Scopus (428) Google Scholar). The Go/NoGo task variant (Figure 3C) is similar to the Immediate-Go task, except that there are three possible instruction cues: Go left, Go right, or hold in place (NoGo). As before, simply holding before the instruction cue was not associated with elevated beta. However, both Go and NoGo cues were similarly followed after several hundred milliseconds by a beta ERS (Figures 3D and 3E). This observation suggests that planning not to move is also associated with enhanced beta and confirms that the main beta ERS that we analyze here is not rigidly linked to either movement initiation or suppression. At the same time, we observed two interesting differences between GO and NOGO trials. First, the beta ERS to the NoGo cue was not followed by the marked ERD seen on GO trials, consistent with a more direct relationship between beta ERD and movement. Second, we noticed that the NoGo cue provoked an additional beta ERS with very low latency, and this was of consistently higher power in the frontal ECoG compared to BG sites (Figure S2C). The Stop-signal task is widely" @default.
• W2042420303 created "2016-06-24" @default.
• W2042420303 creator A5002338541 @default.
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• W2042420303 date "2012-02-01" @default.
• W2042420303 modified "2023-10-15" @default.
• W2042420303 title "Basal Ganglia Beta Oscillations Accompany Cue Utilization" @default.
• W2042420303 cites W1490680688 @default.
• W2042420303 cites W1550030659 @default.
• W2042420303 cites W1632077749 @default.
• W2042420303 cites W1675464103 @default.
• W2042420303 cites W1760402985 @default.
• W2042420303 cites W1890315254 @default.
• W2042420303 cites W1926963061 @default.
• W2042420303 cites W1965586905 @default.
• W2042420303 cites W1969816573 @default.
• W2042420303 cites W1971815199 @default.
• W2042420303 cites W1972681732 @default.
• W2042420303 cites W1975269113 @default.
• W2042420303 cites W1990973912 @default.
• W2042420303 cites W1991271750 @default.
• W2042420303 cites W1992431848 @default.
• W2042420303 cites W1996469777 @default.
• W2042420303 cites W2002648956 @default.
• W2042420303 cites W2002699700 @default.
• W2042420303 cites W2003244414 @default.
• W2042420303 cites W2006874412 @default.
• W2042420303 cites W2010406435 @default.
• W2042420303 cites W2020696324 @default.
• W2042420303 cites W2021583510 @default.
• W2042420303 cites W2023581277 @default.
• W2042420303 cites W2024154387 @default.
• W2042420303 cites W2030345583 @default.
• W2042420303 cites W2035999685 @default.
• W2042420303 cites W2045526770 @default.
• W2042420303 cites W2045839462 @default.
• W2042420303 cites W2048317486 @default.
• W2042420303 cites W2049621655 @default.
• W2042420303 cites W2051572005 @default.
• W2042420303 cites W2053210895 @default.
• W2042420303 cites W2061116526 @default.
• W2042420303 cites W2069166530 @default.
• W2042420303 cites W2075021671 @default.
• W2042420303 cites W2081425074 @default.
• W2042420303 cites W2084147944 @default.
• W2042420303 cites W2085073811 @default.
• W2042420303 cites W2086560561 @default.
• W2042420303 cites W2087822149 @default.
• W2042420303 cites W2088198203 @default.
• W2042420303 cites W2089876605 @default.
• W2042420303 cites W2089965635 @default.
• W2042420303 cites W2095401753 @default.
• W2042420303 cites W2097684433 @default.
• W2042420303 cites W2098526280 @default.
• W2042420303 cites W2101897430 @default.
• W2042420303 cites W2103570990 @default.
• W2042420303 cites W2104625331 @default.
• W2042420303 cites W2104731571 @default.
• W2042420303 cites W2108339789 @default.
• W2042420303 cites W2108676218 @default.
• W2042420303 cites W2110830643 @default.
• W2042420303 cites W2112898018 @default.
• W2042420303 cites W2116600796 @default.
• W2042420303 cites W2116704462 @default.
• W2042420303 cites W2120653271 @default.
• W2042420303 cites W2120768649 @default.
• W2042420303 cites W2124935025 @default.
• W2042420303 cites W2133947591 @default.
• W2042420303 cites W2135681455 @default.
• W2042420303 cites W2137740474 @default.
• W2042420303 cites W2141359096 @default.
• W2042420303 cites W2141405085 @default.
• W2042420303 cites W2144344332 @default.
• W2042420303 cites W2146037001 @default.
• W2042420303 cites W2149555100 @default.
• W2042420303 cites W2150135821 @default.
• W2042420303 cites W2151229057 @default.
• W2042420303 cites W2152891892 @default.
• W2042420303 cites W2155982264 @default.
• W2042420303 cites W2161438629 @default.
• W2042420303 cites W2161472384 @default.
• W2042420303 cites W2162826201 @default.
• W2042420303 cites W2164295765 @default.
• W2042420303 cites W2167683893 @default.
• W2042420303 cites W2170295149 @default.
• W2042420303 cites W2171601518 @default.
• W2042420303 cites W2172257310 @default.
• W2042420303 cites W2186321983 @default.
• W2042420303 cites W2259589351 @default.
• W2042420303 cites W4238789802 @default.
• W2042420303 cites W4297636293 @default.
• W2042420303 doi "https://doi.org/10.1016/j.neuron.2011.11.032" @default.
• W2042420303 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3463873" @default.
• W2042420303 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22325204" @default.

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