Evidence map›Paper›PMID 24843012›Full record

ArticleeLife2014

Midbrain dopamine neurons sustain inhibitory transmission using plasma membrane uptake of GABA, not synthesis.

Nicolas X Tritsch, Won-Jong Oh, Chenghua Gu, Bernardo L Sabatini

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
10.5field-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

130 citing papers in PubMed, 198 citations in OpenAlex.

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  13. Untangling dopamine and glutamate in the ventral tegmental area.bioRxiv : the preprint server for biology · 2025
    Article
  14. Review
  15. Dopamine-Glutamate and Dopamine-GABA Co-release.Advances in neurobiology · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Nicolas X TritschDepartment of Neurobiology, Howard Hughes Medical Institute, Harvard Medical School, Boston, United States.
Won-Jong OhDepartment of Neurobiology, Harvard Medical School, Boston, United States.
Chenghua GuDepartment of Neurobiology, Harvard Medical School, Boston, United States.
Bernardo L SabatiniDepartment of Neurobiology, Howard Hughes Medical Institute, Harvard Medical School, Boston, United States bsabatini@hms.harvard.edu.
Harvard University · US

Funding

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
The Role of Semaphorins in Axon and Blood Vessel GuidanceR01NS064583 · NINDS · HARVARD MEDICAL SCHOOL · PI GU, CHENGHUA · 2010 to 2014
$1.8M
NINDS NIH HHS NS046579NINDS NIH HHS NS064583NINDS NIH HHS R01 NS046579NINDS NIH HHS R01 NS064583NINDS NIH HHS R37 NS046579
6 · The paper itself

Abstract

Synaptic transmission between midbrain dopamine neurons and target neurons in the striatum is essential for the selection and reinforcement of movements. Recent evidence indicates that nigrostriatal dopamine neurons inhibit striatal projection neurons by releasing a neurotransmitter that activates GABAA receptors. Here, we demonstrate that this phenomenon extends to mesolimbic afferents, and confirm that the released neurotransmitter is GABA. However, the GABA synthetic enzymes GAD65 and GAD67 are not detected in midbrain dopamine neurons. Instead, these cells express the membrane GABA transporters mGAT1 (Slc6a1) and mGAT4 (Slc6a11) and inhibition of these transporters prevents GABA co-release. These findings therefore indicate that GABA co-release is a general feature of midbrain dopaminergic neurons that relies on GABA uptake from the extracellular milieu as opposed to de novo synthesis. This atypical mechanism may confer dopaminergic neurons the flexibility to differentially control GABAergic transmission in a target-dependent manner across their extensive axonal arbors.DOI: http://dx.doi.org/10.7554/eLife.01936.001.

Indexed as

Neural InhibitionSynaptic TransmissionAnimalsBiological TransportCorpus StriatumDopaminergic NeuronsGABA AgentsGABA Plasma Membrane Transport Proteinsgamma-Aminobutyric AcidInhibitory Postsynaptic PotentialsMesencephalonMice, Inbred C57BLMice, TransgenicSynapsesTime FactorsGABA AgentsGABA Plasma Membrane Transport Proteinsgamma-Aminobutyric AcidSlc6a11 protein, mouseSlc6a1 protein, mousebasal gangliaco-releasedopamineGABAGATstriatum

Identifiers

PMID24843012
PMCPMC4001323
OpenAlexW2075549646

What OpenQuestion holds

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LicenceCC BY
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.