Evidence map›Paper›PMID 25124148›Full record

ArticleMovement disorders : official journal of the Movement Disorder Society2014

Pallidal gap junctions-triggers of synchrony in Parkinson's disease?

Bettina C Schwab, Tjitske Heida, Yan Zhao, Stephan A van Gils, Richard J A van Wezel

Open access · bronzeAbstract read
In one paragraph

Article in Movement disorders : official journal of the Movement Disorder Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Tremor pathophysiology.Clinical parkinsonism & related disorders · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. On the Role of Arkypallidal and Prototypical Neurons for Phase Transitions in the External Pallidum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  11. Neural field models with transmission delays and diffusion.Journal of mathematical neuroscience · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. The external globus pallidus: progress and perspectives.The European journal of neuroscience · 2016
    Review
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

5 authors at 2 institutions in 1 country.

Bettina C SchwabApplied Analysis, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente, Enschede, The Netherlands; Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente, Enschede, The Netherlands.
Tjitske Heida
Yan Zhao
Stephan A van Gils
Richard J A van Wezel
University of Twente · NLRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although increased synchrony of the neural activity in the basal ganglia may underlie the motor deficiencies exhibited in Parkinson's disease (PD), how this synchrony arises, propagates through the basal ganglia, and changes under dopamine replacement remains unknown. Gap junctions could play a major role in modifying this synchrony, because they show functional plasticity under the influence of dopamine and after neural injury. In this study, confocal imaging was used to detect connexin-36, the major neural gap junction protein, in postmortem tissues of PD patients and control subjects in the putamen, subthalamic nucleus (STN), and external and internal globus pallidus (GPe and GPi, respectively). Moreover, we quantified how gap junctions affect synchrony in an existing computational model of the basal ganglia. We detected connexin-36 in the human putamen, GPe, and GPi, but not in the STN. Furthermore, we found that the number of connexin-36 spots in PD tissues increased by 50% in the putamen, 43% in the GPe, and 109% in the GPi compared with controls. In the computational model, gap junctions in the GPe and GPi strongly influenced synchrony. The basal ganglia became especially susceptible to synchronize with input from the cortex when gap junctions were numerous and high in conductance. In conclusion, connexin-36 expression in the human GPe and GPi suggests that gap junctional coupling exists within these nuclei. In PD, neural injury and dopamine depletion could increase this coupling. Therefore, we propose that gap junctions act as a powerful modulator of synchrony in the basal ganglia.

Indexed as

AgedAged, 80 and overBasal GangliaComputer SimulationConnexinsFemaleGap Junction delta-2 ProteinGap JunctionsGlobus PallidusGlutamate DecarboxylaseHumansMaleMicroscopy, ConfocalModels, NeurologicalParkinson DiseaseConnexinsGap Junction delta-2 ProteinGlutamate Decarboxylaseglutamate decarboxylase 1confocal microscopyConnexin-36globus pallidusoscillations

Identifiers

PMID25124148
PMCPMC4307646
OpenAlexW1914174214

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.