Evidence map›Paper›PMID 25578364›Full record

ArticleNeuron2015

Heterosynaptic regulation of external globus pallidus inputs to the subthalamic nucleus by the motor cortex.

Hong-Yuan Chu, Jeremy F Atherton, David Wokosin, D James Surmeier, Mark D Bevan

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  11. Neuroplasticity in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
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  20. The dendritic engram.Frontiers in behavioral neuroscience · 2023
    Article

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Hong-Yuan ChuDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Jeremy F AthertonDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
David WokosinDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
D James SurmeierDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Mark D BevanDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: m-bevan@northwestern.edu.
Northwestern University · US

Funding

SYNAPTIC CONTROLOF PALLIDAL ACTIVITYP50NS047085 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHUMACKER, PAUL T · 2003 to 2018
$19.2M
Physiology Core - Interdepartmental Two-photon Imaging CenterP30NS054850 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SURMEIER, DALTON JAMES · 2007 to 2012
$3.3M
Synaptic Transmission, Plasticity and Integration in the Subthalamic NucleusR37NS041280 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BEVAN, MARK D · 2012 to 2018
$2.7M
NINDS NIH HHS 2P50 NS047085NINDS NIH HHS 2R37 NS041280NINDS NIH HHS P30 NS054850NINDS NIH HHS P50 NS047085NINDS NIH HHS R37 NS041280
6 · The paper itself

Abstract

The two principal movement-suppressing pathways of the basal ganglia, the so-called hyperdirect and indirect pathways, interact within the subthalamic nucleus (STN). An appropriate level and pattern of hyperdirect pathway cortical excitation and indirect pathway external globus pallidus (GPe) inhibition of the STN are critical for normal movement and are greatly perturbed in Parkinson's disease. Here we demonstrate that motor cortical inputs to the STN heterosynaptically regulate, through activation of postsynaptic NMDA receptors, the number of functional GABAA receptor-mediated GPe-STN inputs. Therefore, a homeostatic mechanism, intrinsic to the STN, balances cortical excitation by adjusting the strength of GPe inhibition. However, following the loss of dopamine, excessive cortical activation of STN NMDA receptors triggers GPe-STN inputs to strengthen abnormally, contributing to the emergence of pathological, correlated activity.

Indexed as

AnimalsDopamineGABAergic Neuronsgamma-Aminobutyric AcidGlobus PallidusGlutamic AcidLong-Term PotentiationMiceMotor CortexNeural PathwaysNeuronal PlasticityOptogeneticsParkinsonian DisordersReceptors, GABA-AReceptors, N-Methyl-D-AspartateSubthalamic NucleusDopaminegamma-Aminobutyric AcidGlutamic AcidReceptors, GABA-AReceptors, N-Methyl-D-Aspartate

Identifiers

PMID25578364
PMCPMC4304914
OpenAlexW1965801504

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.