Dopamine depletion increases the power and coherence of β‐oscillations in the cerebral cortex and subthalamic nucleus of the awake rat

Sharott, Andrew; Magill, Peter J.; Harnack, Daniel; Kupsch, Andreas; Meissner, Wassilios G.; Brown, Peter

doi:10.1111/j.1460-9568.2005.03973.x

Cited by 375 publications

(312 citation statements)

References 68 publications

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“…YKP10A also induced a specific increase in beta-2 activity not observed with the other drugs. Pronounced increases in beta oscillations have also been observed after dopamine depletion in the rat (Sharott et al, 2005). This increase in beta-2 activity combined with YKP10A's clinical profile that resembled that of the drugs known to affect dopamine transmission and preliminary in vitro results (see Introduction) thus lends further support to the notion that this compound affects dopamine signaling.…”

Section: Drug Effects On the Waking Eegsupporting

confidence: 60%

How to Keep the Brain Awake? The Complex Molecular Pharmacogenetics of Wake Promotion

Hasan

Pradervand

Ahnaou³

et al. 2009

Neuropsychopharmacol

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Wake-promoting drugs are widely used to treat excessive daytime sleepiness. The neuronal pathways involved in wake promotion are multiple and often not well characterized. We tested d-amphetamine, modafinil, and YKP10A, a novel wake-promoting compound, in three inbred strains of mice. The wake duration induced by YKP10A and d-amphetamine depended similarly on genotype, whereas opposite strain differences were observed after modafinil. Electroencephalogram (EEG) analysis during drug-induced wakefulness revealed a transient B2 Hz slowing of theta oscillations and an increase in beta-2 (20-35 Hz) activity only after YKP10A. Gamma activity (35-60 Hz) was induced by all drugs in a drug-and genotype-dependent manner. Brain transcriptome and clustering analyses indicated that the three drugs have both common and specific molecular signatures. The correlation between specific EEG and gene-expression signatures suggests that the neuronal pathways activated to stay awake vary among drugs and genetic background.

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Section: Drug Effects On the Waking Eegsupporting

confidence: 60%

How to Keep the Brain Awake? The Complex Molecular Pharmacogenetics of Wake Promotion

Hasan

Pradervand

Ahnaou³

et al. 2009

Neuropsychopharmacol

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“…To further evaluate the changes at specific frequency bands, we calculated the normalized spectrum before, during, and after laser stimulation. We found that optogenetic stimulation of SChIs robustly increased oscillation power across higher frequency bands conventionally defined as alpha (8)(9)(10)(11)(12)(13)(14)(15), beta (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), low gamma (30-60 Hz), and high gamma (60-100 Hz), but not lower frequency bands of delta (1-4 Hz) or theta (4-8 Hz) (Fig. 2 E and F; n = 7 mice).…”

Section: Resultsmentioning

confidence: 99%

“…A hallmark of PD pathology is chronic reduction of dopamine input to CBT circuits due to midbrain dopaminergic neuron loss. Loss of midbrain dopamine increases beta oscillation power and coherence in PD animal models (14,15). Similarly, acute reduction of dopamine locally in the striatum increases striatal beta oscillations (16).…”

mentioning

confidence: 99%

Striatal cholinergic interneurons generate beta and gamma oscillations in the corticostriatal circuit and produce motor deficits

Kondabolu

Roberts

Bucklin

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Cortico-basal ganglia-thalamic (CBT) neural circuits are critical modulators of cognitive and motor function. When compromised, these circuits contribute to neurological and psychiatric disorders, such as Parkinson's disease (PD). In PD, motor deficits correlate with the emergence of exaggerated beta frequency (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) oscillations throughout the CBT network. However, little is known about how specific cell types within individual CBT brain regions support the generation, propagation, and interaction of oscillatory dynamics throughout the CBT circuit or how specific oscillatory dynamics are related to motor function. Here, we investigated the role of striatal cholinergic interneurons (SChIs) in generating beta and gamma oscillations in cortical-striatal circuits and in influencing movement behavior. We found that selective stimulation of SChIs via optogenetics in normal mice robustly and reversibly amplified beta and gamma oscillations that are supported by distinct mechanisms within striatal-cortical circuits. Whereas beta oscillations are supported robustly in the striatum and all layers of primary motor cortex (M1) through a muscarinic-receptor mediated mechanism, gamma oscillations are largely restricted to the striatum and the deeper layers of M1. Finally, SChI activation led to parkinsonianlike motor deficits in otherwise normal mice. These results highlight the important role of striatal cholinergic interneurons in supporting oscillations in the CBT network that are closely related to movement and parkinsonian motor symptoms.E xaggerated beta oscillations (15-30 Hz) within the cortico-basal ganglia-thalamic (CBT) neural network are putative electrophysiological correlates of bradykinesia and rigidity in Parkinson's disease (PD) (1-4). Therapies that effectively manage PD motor symptoms, such as dopamine replacement therapy and deep brain stimulation, are associated with a suppression of the exaggerated beta oscillations (4, 5). Beta oscillations are also found in the CBT circuits of patients with other movement-related disorders, such as epilepsy and dystonia (6, 7), and in normal, nonhuman primates (8, 9) and normal rodents (10, 11). Moreover, brief elevations (≤200 ms) of beta oscillations are observed in the basal ganglia of task-performing nonhuman primates and rodents during specific phases of behavioral tasks (10, 12, 13), indicating that beta oscillations may be important for motor and nonmotor functions. In contrast to the regulated temporal variability of beta oscillations in normal motor functions, temporal stability is correlated with the parkinsonian motor symptoms of bradykinesia and rigidity (2). Together, these findings suggest that brief epochs of beta oscillations are a normal aspect of basal ganglia dynamics, their temporal modulation is important for movement regulation, and loss of regulation or uncontrolled expression of beta oscillations may contribute to movement deficits, such as those observed in PD.Despite the clear link bet...

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“…Dopaminergic medication and active movements are known to decrease STN beta synchronization (Brown et al 2001;Foffani et al 2005;Kuhn et al 2004;Levy et al 2002;Marsden et al 2001b;Priori et al 2002Priori et al , 2004 and deep brain stimulation in the STN may alleviate PD symptoms by disrupting this oscillatory activity (Brown et al 2004;Filali et al 2004;Jahanshahi et al 2000;Lozano et al 2002). It was previously hypothesized that dopamine action on the striatum acts as a filter for cortical input to the STN (Doyle et al 2005;Magill et al 2001Magill et al , 2004Sharott et al 2005). Thus the increase in number of STN cells with oscillatory beta activity might reflect the degree of nigrostriatal dopamine deficiency.…”

Section: Discussionmentioning

confidence: 99%

Beta Oscillatory Activity in the Subthalamic Nucleus and Its Relation to Dopaminergic Response in Parkinson's Disease

Weinberger

Mahant²,

Hutchison³

et al. 2006

Journal of Neurophysiology

540

389

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. Beta oscillatory activity in the subthalamic nucleus and its relation to dopaminergic response in Parkinson's disease. J Neurophysiol 96: 3248 -3256, 2006. First published September 27, 2006 doi:10.1152/jn.00697.2006. Recent studies suggest that beta (15-30 Hz) oscillatory activity in the subthalamic nucleus (STN) is dramatically increased in Parkinson's disease (PD) and may interfere with movement execution. Dopaminergic medications decrease beta activity and deep brain stimulation (DBS) in the STN may alleviate PD symptoms by disrupting this oscillatory activity. Depth recordings from PD patients have demonstrated beta oscillatory neuronal and local field potential (LFP) activity in STN, although its prevalence and relationship to neuronal activity are unclear. In this study, we recorded both LFP and neuronal spike activity from the STN in 14 PD patients during functional neurosurgery. Of 200 singleand multiunit recordings 56 showed significant oscillatory activity at about 26 Hz and 89% of these were coherent with the simultaneously recorded LFP. The incidence of neuronal beta oscillatory activity was significantly higher in the dorsal STN (P ϭ 0.01) and corresponds to the significantly increased LFP beta power recorded in the same region. Of particular interest was a significant positive correlation between the incidence of oscillatory neurons and the patient's benefit from dopaminergic medications, but not with baseline motor deficits off medication. These findings suggest that the degree of neuronal beta oscillatory activity is related to the magnitude of the response of the basal ganglia to dopaminergic agents rather than directly to the motor symptoms of PD. The study also suggests that LFP beta oscillatory activity is generated largely within the dorsal portion of the STN and can produce synchronous oscillatory activity of the local neuronal population.

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Dopamine depletion increases the power and coherence of β‐oscillations in the cerebral cortex and subthalamic nucleus of the awake rat

Cited by 375 publications

References 68 publications

How to Keep the Brain Awake? The Complex Molecular Pharmacogenetics of Wake Promotion

How to Keep the Brain Awake? The Complex Molecular Pharmacogenetics of Wake Promotion

Striatal cholinergic interneurons generate beta and gamma oscillations in the corticostriatal circuit and produce motor deficits

Beta Oscillatory Activity in the Subthalamic Nucleus and Its Relation to Dopaminergic Response in Parkinson's Disease

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