Evidence map›Paper›PMID 25552639›Full record

ArticleJournal of neurophysiology2015

Nigral dopamine loss induces a global upregulation of presynaptic dopamine D1 receptor facilitation of the striatonigral GABAergic output.

Shengyuan Ding, Li Li, Fu-Ming Zhou

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

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  17. The Basal Ganglia in Action.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2017
    Review
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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

3 authors at 1 institution in 1 country.

Shengyuan DingDepartment of Pharmacology, University of Tennessee College of Medicine, Memphis, Tennessee.
Li LiDepartment of Pharmacology, University of Tennessee College of Medicine, Memphis, Tennessee.
Fu-Ming ZhouDepartment of Pharmacology, University of Tennessee College of Medicine, Memphis, Tennessee fzhou3@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

Regulation of basal ganglia output neuronsR01NS058850 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ZHOU, FU-MING · 2008 to 2012
$1.3M
NINDS NIH HHS R01 NS058850NINDS NIH HHS R01-NS-058850
6 · The paper itself

Abstract

In Parkinson's disease (PD), the dopamine (DA) neuron loss in the substantia nigra and the DA axon loss in the dorsal striatum are severe, but DA neurons in the ventral tegmental area and DA axons in middle and ventral striatal subregions are less affected. Severe DA loss leads to DA receptor supersensitivity, but it was not known whether the supersensitivity of the DA D1 receptors (D1Rs) on the striatonigral axon terminal is determined by the severe striatal or nigral DA loss. This question is important because these two possibilities affect the extent of the striatonigral terminals with supersensitive D1Rs and hence the strength of the direct pathway output. Here we have investigated this question in the transcription factor Pitx3 mutant mice that have a PD-like DA loss pattern. We found that the presynaptic D1R function was upregulated globally: the D1R-mediated facilitation was equally enhanced for the striatonigral GABA output originated in the dorsal striatum where the DA loss is severe and the somatic D1Rs are supersensitive, and for the striatonigral GABA output originated in the middle and ventral striatum where the DA loss is moderate and the somatic D1Rs are not supersensitive. These results suggest that severe nigral DA loss is sufficient to induce functional upregulation of the D1Rs on striatonigral axon terminals. Consequently, in PD, the globally enhanced D1Rs on striatonigral axon terminals originated in broad striatal subregions may strongly enhance the striatonigral GABA output upon D1R stimulation, potentially contributing to D1R agonism's profound motor-stimulating effects.

Indexed as

Up-RegulationAnimalsDopaminegamma-Aminobutyric AcidHomeodomain ProteinsMiceReceptors, Dopamine D1Substantia NigraSynapsesTranscription FactorsDopaminegamma-Aminobutyric Acidhomeobox protein PITX3Homeodomain ProteinsReceptors, Dopamine D1Transcription Factorsbasal gangliadopamine receptor supersensitivityl-3,4-dihydroxyphenylalanine (l-dopa)Parkinson's diseasesubstantia nigra

Identifiers

PMID25552639
PMCPMC4359993
OpenAlexW2128280881

What OpenQuestion holds

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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.