Evidence map›Paper›PMID 24051279›Full record

ArticleNeurobiology of disease2014

Axonal and synaptic failure suppress the transfer of firing rate oscillations, synchrony and information during high frequency deep brain stimulation.

Robert Rosenbaum, Andrew Zimnik, Fang Zheng, Robert S Turner, Christian Alzheimer, Brent Doiron, Jonathan E Rubin

Abstract read
In one paragraph

Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
–field-weighted citation impact
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

59 citing papers in PubMed.

  1. Article
  2. Recovery of Dexterous Motor Control via Non-Monosynaptic Corticospinal Pathways.medRxiv : the preprint server for health sciences · 2026
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  10. Review
  11. The Therapeutic Frequency Profile of Subthalamic Nucleus Deep Brain Stimulation in Rats Is Shaped by Antidromic Spike Failure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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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.

Robert RosenbaumDepartment of Mathematics, University of Pittsburgh, Pittsburgh, PA, USA; Center for the Neural Basis of Cognition, Pittsburgh, PA, USA. Electronic address: robertr@pitt.edu.
Andrew ZimnikDepartment of Neurobiology, University of Pittsburgh, Pittsburgh, PA, USA.
Fang ZhengInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Germany.
Robert S TurnerCenter for the Neural Basis of Cognition, Pittsburgh, PA, USA; Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA, USA.
Christian AlzheimerInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Germany.
Brent DoironDepartment of Mathematics, University of Pittsburgh, Pittsburgh, PA, USA; Center for the Neural Basis of Cognition, Pittsburgh, PA, USA.
Jonathan E RubinDepartment of Mathematics, University of Pittsburgh, Pittsburgh, PA, USA; Center for the Neural Basis of Cognition, Pittsburgh, PA, USA.

Funding

Basal ganglia-thalamic signaling in parkinsonism and deep brain stimulationR01NS070865 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TURNER, ROBERT STERLING · 2011 to 2015
$1.8M
Surgery Core - NINDS Institutional Core Grants to Support Neuroscience ResearchP30NS076405 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STRICK, PETER · 2012 to 2016
$1.8M
NINDS NIH HHS P30 NS076405NINDS NIH HHS R01 NS070865
6 · The paper itself

Abstract

High frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a widely used treatment for Parkinson's disease, but its effects on neural activity in basal ganglia circuits are not fully understood. DBS increases the excitation of STN efferents yet decouples STN spiking patterns from the spiking patterns of STN synaptic targets. We propose that this apparent paradox is resolved by recent studies showing an increased rate of axonal and synaptic failures in STN projections during DBS. To investigate this hypothesis, we combine in vitro and in vivo recordings to derive a computational model of axonal and synaptic failure during DBS. Our model shows that these failures induce a short term depression that suppresses the synaptic transfer of firing rate oscillations, synchrony and rate-coded information from STN to its synaptic targets. In particular, our computational model reproduces the widely reported suppression of parkinsonian β oscillations and synchrony during DBS. Our results support the idea that short term depression is a therapeutic mechanism of STN DBS that works as a functional lesion by decoupling the somatic spiking patterns of STN neurons from spiking activity in basal ganglia output nuclei.

Indexed as

Deep Brain StimulationAction PotentialsAnimalsAxonsComputer SimulationDopaminergic NeuronsGlobus PallidusMacaca mulattaMaleModels, NeurologicalNeural PathwaysRatsRats, WistarSubstantia NigraSubthalamic NucleusSynapsesAxonal failureBeta oscillationsDeep brain stimulationParkinson's diseaseShort term depressionSynaptic failure

Identifiers

PMID24051279
PMCPMC3877705

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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.