Evidence map›Paper›PMID 24966377›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Striatal cholinergic neurotransmission requires VGLUT3.

Alexandra B Nelson, Timothy G Bussert, Anatol C Kreitzer, Rebecca P Seal

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Dual cholinergic mechanisms for sculpting striatal dopamine in vivo.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. VGLUT3 Deletion Rescues Motor Deficits and Neuronal Loss in the zQ175 Mouse Model of Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Functional dissociation of behavioral effects from acetylcholine and glutamate released from cholinergic striatal interneurons.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  16. Review
  17. From Progenitors to Progeny: Shaping Striatal Circuit Development and Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  18. Er81 Transcription Factor Fine-Tunes Striatal Cholinergic Interneuron Activity and Drives Habit Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  19. Functional Connectome Analysis of the Striatum with Optogenetics.Advances in experimental medicine and biology · 2021
    Article
  20. Article

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

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

4 authors at 3 institutions in 1 country.

Alexandra B NelsonGladstone Institute for Neurological Disease, J. David Gladstone Institutes, San Francisco, California 94158, Department of Neurology, University of California, San Francisco 94117.
Timothy G BussertDepartment of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, and.
Anatol C KreitzerGladstone Institute for Neurological Disease, J. David Gladstone Institutes, San Francisco, California 94158, Department of Neurology, University of California, San Francisco 94117, Department of Physiology, University of California at San Francisco, San Francisco, California 94117 rpseal@pitt.edu akreitzer@gladstone.ucsf.edu.
Rebecca P SealDepartment of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, and rpseal@pitt.edu akreitzer@gladstone.ucsf.edu.
University of Pittsburgh · USGladstone Institutes · USUniversity of California, San Francisco · US

Funding

Neuron- and Circuit-Specific Mechanisms and Adaptations Regulating Striatal FunctR01NS064984 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI KREITZER, ANATOL · 2009 to 2022
$5.1M
Striatal Neuroplasticity Mechanisms that Preserve Motor Behavior in a model of Parkinson’s DiseaseR01NS082650 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SEAL, REBECCA P · 2013 to 2023
$4.0M
Striatal Microcircuits: Regulation and FunctionR01NS078435 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERKE, JOSHUA D, KREITZER, ANATOL · 2012 to 2016
$2.4M
Optogenetic dissection of striatal circuits in a mouse model of human dystoniaK08NS081001 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NELSON, ALEXANDRA · 2012 to 2016
$858k
NINDS NIH HHS K08 NS081001NINDS NIH HHS R01 NS064984NINDS NIH HHS R01 NS078435NINDS NIH HHS R01 NS082650
6 · The paper itself

Abstract

It is now clear that many neuronal populations release more than one classical neurotransmitter, yet in most cases the functional role of corelease is unknown. Striatal cholinergic interneurons release both glutamate and acetylcholine, and vesicular loading of glutamate has been shown to enhance acetylcholine content. Using a combination of optogenetics and whole-cell recordings in mice, we now provide physiological evidence that optogenetic stimulation of cholinergic interneurons triggers monosynaptic glutamate- and acetylcholine-mediated currents in striatal fast-spiking interneurons (FSIs), both of which depend on the expression of the vesicular glutamate transporter 3 (VGLUT3). In contrast to corticostriatal glutamatergic inputs onto FSIs, which are mediated primarily by AMPA-type glutamate receptors, glutamate release by cholinergic interneurons activates both AMPA- and NMDA-type glutamate receptors, suggesting a unique role for these inputs in the modulation of FSI activity. Importantly, we find that the loss of VGLUT3 not only markedly attenuates glutamatergic and cholinergic inputs on FSIs, but also significantly decreases disynaptic GABAergic input onto medium spiny neurons (MSNs), the major output neurons of the striatum. Our data demonstrate that VGLUT3 is required for normal cholinergic signaling onto FSIs, as well as for acetylcholine-dependent disynaptic inhibition of MSNs. Thus, by supporting fast glutamatergic transmission as well as by modulating the strength of cholinergic signaling, VGLUT3 has the capacity to exert widespread influence on the striatal network.

Indexed as

AcetylcholineAmino Acid Transport Systems, AcidicAnimalsCholinergic NeuronsCorpus StriatumGlutamic AcidInterneuronsMiceMice, TransgenicSynaptic TransmissionAcetylcholineAmino Acid Transport Systems, AcidicGlutamic AcidSlc17a8 protein, mouseacetylcholinecoreleasefast-spiking interneuronglutamatestriatumVGLUT3

Identifiers

PMID24966377
PMCPMC4069355
OpenAlexW2170258699

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.