Evidence map›Paper›PMID 27566978›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

Cortical Control of Striatal Dopamine Transmission via Striatal Cholinergic Interneurons.

Polina Kosillo, Yan-Feng Zhang, Sarah Threlfell, Stephanie J Cragg

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. The Cellular and Synaptic Actions of Dopamine During Behavior.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Dual cholinergic mechanisms for sculpting striatal dopamine in vivo.bioRxiv : the preprint server for biology · 2025
    Article
  14. Article
  15. Article
  16. mGlu2 Receptors in the Basal Ganglia: A New Frontier in Addiction Therapy.Frontiers in bioscience (Landmark edition) · 2025
    Review
  17. Levodopa treatment: impacts and mechanisms throughout Parkinson's disease progression.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  18. Article
  19. Article
  20. Article

47 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 2 institutions in 2 countries.

Polina KosilloDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK.
Yan-Feng ZhangDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK.
Sarah ThrelfellDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK.
Stephanie J CraggDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK.
University of Oxford · GBUniversity of California, Berkeley · US

Funding

Medical Research Council G0700932Medical Research Council MR/J004324/1Medical Research Council MR/K013866/1Parkinson's UK G-0803Parkinson's UK G-0808Parkinson's UK G-1103Parkinson's UK G-1305Parkinson's UK J-0901
6 · The paper itself

Abstract

Corticostriatal regulation of striatal dopamine (DA) transmission has long been postulated, but ionotropic glutamate receptors have not been localized directly to DA axons. Striatal cholinergic interneurons (ChIs) are emerging as major players in striatal function, and can govern DA transmission by activating nicotinic receptors (nAChRs) on DA axons. Cortical inputs to ChIs have historically been perceived as sparse, but recent evidence indicates that they strongly activate ChIs. We explored whether activation of M1/M2 corticostriatal inputs can consequently gate DA transmission, via ChIs. We reveal that optogenetic activation of channelrhodopsin-expressing corticostriatal axons can drive striatal DA release detected with fast-scan cyclic voltammetry and requires activation of nAChRs on DA axons and AMPA receptors on ChIs that promote short-latency action potentials. By contrast, DA release driven by optogenetic activation of intralaminar thalamostriatal inputs involves additional activation of NMDA receptors on ChIs and action potential generation over longer timescales. Therefore, cortical and thalamic glutamate inputs can modulate DA transmission by regulating ChIs as gatekeepers, through ionotropic glutamate receptors. The different use of AMPA and NMDA receptors by cortical versus thalamic inputs might lead to distinct input integration strategies by ChIs and distinct modulation of the function of DA and striatum.

Indexed as

AMPA receptorcorticostriatalNMDA receptorthalamostriatalvoltammetry

Identifiers

PMID27566978
PMCPMC5066833
OpenAlexW2517992311

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.