Evidence map›Paper›PMID 23034651›Full record

ArticleNature2012

Dopaminergic neurons inhibit striatal output through non-canonical release of GABA.

Nicolas X Tritsch, Jun B Ding, Bernardo L Sabatini

Open access · greenAbstract read
In one paragraph

Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 377 papers.

0numbers the graph read from it
0cells of the map it votes in
377citing papers in PubMed
17.0field-weighted citation impact, top 1% 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

377 citing papers in PubMed, 591 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Article
  7. Review
  8. Dopamine modulation of aggression.Psychopharmacology · 2026
    Review
  9. Article
  10. Gut-Brain Signaling in Parkinson's Disease: A Narrative Review.International journal of molecular sciences · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. ImmatureProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  17. Article
  18. Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Nicolas X TritschDepartment of Neurobiology, Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.
Jun B Ding
Bernardo L Sabatini
Harvard University · USHoward Hughes Medical Institute · USStanford University · US

Funding

FUNDAMENTAL NEUROBIOLOGYT32NS007484 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI REGEHR, WADE G · 2000 to 2014
$5.9M
Dendritic Ca signals in striatal medium spiny neuronsR01NS046579 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SABATINI, BERNARDO L · 2004 to 2016
$5.0M
Action and interaction of ionotropic and metabotropic neurotransmissionR37NS046579 · NINDS · HARVARD MEDICAL SCHOOL · PI SABATINI, BERNARDO L · 2018 to 2024
$4.6M
Functional organization of neural circuits underlying movement controlR00NS075136 · NINDS · STANFORD UNIVERSITY · PI DING, JUN · 2012 to 2014
$727k
Howard Hughes Medical InstituteNINDS NIH HHS 4R00NS075136NINDS NIH HHS NS046579NINDS NIH HHS R00 NS075136NINDS NIH HHS R01 NS046579NINDS NIH HHS R37 NS046579NINDS NIH HHS T32 NS007484
6 · The paper itself

Abstract

The substantia nigra pars compacta and ventral tegmental area contain the two largest populations of dopamine-releasing neurons in the mammalian brain. These neurons extend elaborate projections in the striatum, a large subcortical structure implicated in motor planning and reward-based learning. Phasic activation of dopaminergic neurons in response to salient or reward-predicting stimuli is thought to modulate striatal output through the release of dopamine to promote and reinforce motor action. Here we show that activation of dopamine neurons in striatal slices rapidly inhibits action potential firing in both direct- and indirect-pathway striatal projection neurons through vesicular release of the inhibitory transmitter GABA (γ-aminobutyric acid). GABA is released directly from dopaminergic axons but in a manner that is independent of the vesicular GABA transporter VGAT. Instead, GABA release requires activity of the vesicular monoamine transporter VMAT2, which is the vesicular transporter for dopamine. Furthermore, VMAT2 expression in GABAergic neurons lacking VGAT is sufficient to sustain GABA release. Thus, these findings expand the repertoire of synaptic mechanisms used by dopamine neurons to influence basal ganglia circuits, show a new substrate whose transport is dependent on VMAT2 and demonstrate that GABA can function as a bona fide co-transmitter in monoaminergic neurons.

Indexed as

AnimalsCorpus StriatumDopaminergic NeuronsGABA Plasma Membrane Transport Proteinsgamma-Aminobutyric AcidGene Expression ProfilingGene Expression RegulationGene Knock-In TechniquesMiceMice, TransgenicVesicular Monoamine Transport ProteinsGABA Plasma Membrane Transport Proteinsgamma-Aminobutyric AcidSlc18a2 protein, mouseVesicular Monoamine Transport Proteins

Identifiers

PMID23034651
PMCPMC3944587
OpenAlexW2139495058

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.