Evidence map›Paper›PMID 22209920›Full record

ArticleNeuroscience2012

Frequency selectivity and dopamine-dependence of plasticity at glutamatergic synapses in the subthalamic nucleus.

N Yamawaki, P J Magill, G L Woodhall, S D Hall, I M Stanford

Open access · bronzeAbstract read
In one paragraph

Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  12. Mechanisms of deep brain stimulation.Journal of neurophysiology · 2016
    Review
  13. NMDA Receptors Containing the GluN2D Subunit Control Neuronal Function in the Subthalamic Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  14. Article
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  16. Review
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  19. Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  20. 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

5 authors at 2 institutions in 1 country.

N YamawakiAston Brain Centre, School of Life and Health Sciences, Aston University, Birmingham, UK.
P J Magill
G L Woodhall
S D Hall
I M Stanford
Aston University · GBMedical Research Council · GB

Funding

Medical Research Council MC_U138197109
6 · The paper itself

Abstract

In Parkinson's disease, subthalamic nucleus (STN) neurons burst fire with increased periodicity and synchrony. This may entail abnormal release of glutamate, the major source of which in STN is cortical afferents. Indeed, the cortico-subthalamic pathway is implicated in the emergence of excessive oscillations, which are reduced, as are symptoms, by dopamine-replacement therapy or deep brain stimulation (DBS) targeted to STN. Here we hypothesize that glutamatergic synapses in the STN may be differentially modulated by low-frequency stimulation (LFS) and high-frequency stimulation (HFS), the latter mimicking deep brain stimulation. Recordings of evoked and spontaneous excitatory post synaptic currents (EPSCs) were made from STN neurons in brain slices obtained from dopamine-intact and chronically dopamine-depleted adult rats. HFS had no significant effect on evoked (e) EPSC amplitude in dopamine-intact slices (104.4±8.0%) but depressed eEPSCs in dopamine-depleted slices (67.8±6.2%). Conversely, LFS potentiated eEPSCs in dopamine-intact slices (126.4±8.1%) but not in dopamine-depleted slices (106.7±10.0%). Analyses of paired-pulse ratio, coefficient of variation, and spontaneous EPSCs suggest that the depression and potentiation have a presynaptic locus of expression. These results indicate that the synaptic efficacy in dopamine-intact tissue is enhanced by LFS. Furthermore, the synaptic efficacy in dopamine-depleted tissue is depressed by HFS. Therefore the therapeutic effects of DBS in Parkinson's disease appear mediated, in part, by glutamatergic cortico-subthalamic synaptic depression and implicate dopamine-dependent increases in the weight of glutamate synapses, which would facilitate the transfer of pathological oscillations from the cortex.

Indexed as

AnimalsDopamineElectric StimulationExcitatory Postsynaptic PotentialsGlutamic AcidMaleNeuronal PlasticityNeuronsOrgan Culture TechniquesOxidopamineParkinson Disease, SecondaryRatsRats, WistarSubthalamic NucleusSynapsesSynaptic TransmissionDopamineGlutamic AcidOxidopamine

Identifiers

PMID22209920
PMCPMC4245479
OpenAlexW2081270891

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.