Evidence map›Paper›PMID 28526611›Full record

ArticleNeuropharmacology2017

Alcohol induces input-specific aberrant synaptic plasticity in the rat dorsomedial striatum.

Tengfei Ma, Britton Barbee, Xuehua Wang, Jun Wang

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  6. Article
  7. An emerging role for synaptic ZnPharmacology & therapeutics · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025
    Review
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Tengfei MaDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, TX, USA.
Britton BarbeeDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, TX, USA.
Xuehua WangDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, TX, USA.
Jun WangDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, TX, USA. Electronic address: jwang@medicine.tamhsc.edu.
Texas A&M Health Science Center · US

Funding

Prenatal microRNA neuro-therapeutics for fetal alcohol exposureR01AA024659 · NIAAA · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MIRANDA, RAJESH C · 2016 to 2020
$1.8M
Ethanol and glutamatergic transmission in the dorsal striatumR01AA021505 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WANG, JUN · 2012 to 2016
$1.4M
NIAAA NIH HHS R01 AA021505NIAAA NIH HHS R01 AA024659
6 · The paper itself

Abstract

Accumulated evidence suggests that the dorsomedial striatum (DMS) of the basal ganglia plays an essential role in pathological excessive alcohol consumption. The DMS receives multiple glutamatergic inputs. However, whether and how alcohol consumption distinctly affects these excitatory afferents to the DMS remains unknown. Here, we used optogenetics to selectively activate the rat medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) inputs in DMS slices, and measured the effects of alcohol consumption on glutamatergic transmission in these corticostriatal and amygdalostriatal circuits. We found that excessive alcohol consumption increased AMPA receptor- and NMDA receptor (NMDAR)-mediated neurotransmission, as well as the GluN2B/NMDAR ratio, at the corticostriatal input to the DMS. The probability of glutamate release was increased selectively at the amygdalostriatal input. Interestingly, we discovered that paired activation of the mPFC and BLA inputs using dual-channel optogenetics induced robust long-term potentiation (LTP) of the corticostriatal input to the DMS. Taken together, these results indicate that excessive alcohol consumption potentiates glutamatergic transmission via a postsynaptic mechanism for the corticostriatal input and via a presynaptic mechanism for the amygdalostriatal input. These changes may in turn contribute to pathological alcohol consumption.

Indexed as

AnimalsBasolateral Nuclear ComplexCentral Nervous System DepressantsCorpus StriatumEthanolGlutamic AcidMaleNeural PathwaysNeuronal PlasticityOptogeneticsPrefrontal CortexRats, Long-EvansReceptors, GlutamateSynapsesTissue Culture TechniquesCentral Nervous System DepressantsEthanolGlutamic AcidReceptors, GlutamateBasolateral amygdalaDorsomedial striatumEthanolGlutamatergic receptorMedial prefrontal cortexOptogenetics

Identifiers

PMID28526611
PMCPMC5531610
OpenAlexW2615775020

What OpenQuestion holds

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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.