Evidence map›Paper›PMID 26586558›Full record

ArticleNeurobiology of disease2016

Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease.

Kristin B Dupre, Ana V Cruz, Alex J McCoy, Claire Delaville, Colin M Gerber, Katherine W Eyring, Judith R Walters

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.5field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  8. Distinctive Effects of D1 and D2 Receptor Agonists on Cortico-Basal Ganglia Oscillations in a Rodent Model of L-DOPA-Induced Dyskinesia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
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  10. Translational Model of Cortical Premotor-Motor Networks.Cerebral cortex (New York, N.Y. : 1991) · 2022
    Article
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  19. Review
  20. Enhancing Gamma Oscillations Restores Primary Motor Cortex Plasticity in Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kristin B DupreNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States.
Ana V CruzNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States.
Alex J McCoyNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States.
Claire DelavilleNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States.
Colin M GerberNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States.
Katherine W EyringNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States.
Judith R WaltersNeurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892-3702, United States. Electronic address: waltersj@ninds.nih.gov.
National Institutes of Health · US

Funding

Pharmacology And Physiology Of The Substantia Nigra And Basal GangliaZIANS002139 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WALTERS, JUDITH RICHMOND · 2009 to 2021
$14.3M
Thalamo-Cortical Plasticity: Sensory Denervation and Loss of DopamineZIANS003117 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WALTERS, JUDITH RICHMOND · 2010 to 2021
$8.8M
PHARMACOLOGY AND PHYSIOLOGY OF THE SUBSTANTIA NIGRA AND BASAL GANGLIAZ01NS002139 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI WALTERS, JUDITH RICHMOND · 1985 to 2008
$3.4M
Intramural NIH HHS Z01 NS002139
6 · The paper itself

Abstract

Prolonged L-dopa treatment in Parkinson's disease (PD) often leads to the expression of abnormal involuntary movements known as L-dopa-induced dyskinesia. Recently, dramatic 80 Hz oscillatory local field potential (LFP) activity within the primary motor cortex has been linked to dyskinetic symptoms in a rodent model of PD and attributed to stimulation of cortical dopamine D1 receptors. To characterize the relationship between high gamma (70-110 Hz) cortical activity and the development of L-dopa-induced dyskinesia, cortical LFP and spike signals were recorded in hemiparkinsonian rats treated with L-dopa for 7 days, and dyskinesia was quantified using the abnormal involuntary movements (AIMs) scale. The relationship between high gamma and dyskinesia was further probed by assessment of the effects of pharmacological agents known to induce or modulate dyskinesia expression. Findings demonstrate that AIMs and high gamma LFP power increase between days 1 and 7 of L-dopa priming. Notably, high beta (25-35 Hz) power associated with parkinsonian bradykinesia decreased as AIMs and high gamma LFP power increased during priming. After priming, rats were treated with the D1 agonist SKF81297 and the D2 agonist quinpirole. Both dopamine agonists independently induced AIMs and high gamma cortical activity that were similar to that induced by L-dopa, showing that this LFP activity is neither D1 nor D2 receptor specific. The serotonin 1A receptor agonist 8-OH-DPAT reduced L-dopa- and DA agonist-induced AIMs and high gamma power to varying degrees, while the serotonin 1A antagonist WAY100635 reversed these effects. Unexpectedly, as cortical high gamma power increased, phase locking of cortical pyramidal spiking to high gamma oscillations decreased, raising questions regarding the neural substrate(s) responsible for high gamma generation and the functional correlation between high gamma and dyskinesia.

Indexed as

8-Hydroxy-2-(di-n-propylamino)tetralinAnimalsBenzazepinesDisease Models, AnimalDopamine AgonistsDyskinesia, Drug-InducedGamma RhythmLevodopaMaleMotor ActivityMotor CortexNeuronsOxidopamineParkinsonian DisordersQuinpiroleRats8-Hydroxy-2-(di-n-propylamino)tetralinBenzazepinesDopamine AgonistsLevodopaOxidopamineQuinpiroleSerotonin Receptor AgonistsSK&F 81297Abnormal involuntary movementsBetaDopamineDyskinesiaGammaL-dopaLocal field potentialMotor cortexOscillationsParkinson's disease

Identifiers

PMID26586558
PMCPMC5035152
OpenAlexW2173666493

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.