Evidence map›Paper›PMID 23945778›Full record

ArticleJournal of neurophysiology2013

Supersensitive presynaptic dopamine D2 receptor inhibition of the striatopallidal projection in nigrostriatal dopamine-deficient mice.

Wei Wei, Li Li, Guoliang Yu, Shengyuan Ding, Chengyao Li, Fu-Ming Zhou

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  9. Striatal Indirect Pathway Dysfunction Underlies Motor Deficits in a Mouse Model of Paroxysmal Dyskinesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    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

6 authors at 2 institutions in 2 countries.

Wei WeiDepartment of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee; and.
Li Li
Guoliang Yu
Shengyuan Ding
Chengyao Li
Fu-Ming Zhou
University of Tennessee Health Science Center · USSouthern Medical University · CN

Funding

Regulation of basal ganglia output neuronsR01NS058850 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ZHOU, FU-MING · 2008 to 2012
$1.3M
Supersensitive dopamine D2 receptor inhibition of the striatopallidal projectionR03NS085380 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ZHOU, FU-MING · 2013 to 2014
$149k
NINDS NIH HHS R01 NS-058850NINDS NIH HHS R03 NS-085380NINDS NIH HHS R03 NS085380
6 · The paper itself

Abstract

The dopamine (DA) D2 receptor (D2R)-expressing medium spiny neurons (D2-MSNs) in the striatum project to and inhibit the GABAergic neurons in the globus pallidus (GP), forming an important link in the indirect pathway of the basal ganglia movement control circuit. These striatopallidal axon terminals express presynaptic D2Rs that inhibit GABA release and thus regulate basal ganglion function. Here we show that in transcription factor Pitx3 gene mutant mice with a severe DA loss in the dorsal striatum mimicking the DA denervation in Parkinson's disease (PD), the striatopallidal GABAergic synaptic transmission displayed a heightened sensitivity to presynaptic D2R-mediated inhibition with the dose-response curve shifted to the left, although the maximal inhibition was not changed. Functionally, low concentrations of DA were able to more efficaciously reduce the striatopallidal inhibition-induced pauses of GP neuron activity in DA-deficient Pitx3 mutant mice than in wild-type mice. These results demonstrate that presynaptic D2R inhibition of the striatopallidal synapse becomes supersensitized after DA loss. These supersensitive D2Rs may compensate for the lost DA in PD and also induce a strong disinhibition of GP neuron activity that may contribute to the motor-stimulating effects of dopaminergic treatments in PD.

Indexed as

Inhibitory Postsynaptic PotentialsAction PotentialsAnimalsDopamineDopaminergic NeuronsGABAergic NeuronsGlobus PallidusHomeodomain ProteinsMiceMice, Mutant StrainsMutationPresynaptic TerminalsReceptors, Dopamine D2Substantia NigraTranscription FactorsDopaminehomeobox protein PITX3Homeodomain ProteinsReceptors, Dopamine D2Transcription Factorsbasal gangliadopamine receptorglobus pallidusParkinson's diseasepresynaptic inhibition

Identifiers

PMID23945778
PMCPMC3841926
OpenAlexW2080200347

What OpenQuestion holds

Textmetadata
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.