Evidence map›Paper›PMID 27906494›Full record

ReviewGenes, brain, and behavior2017

Alcohol-dependent molecular adaptations of the NMDA receptor system.

N Morisot, D Ron

Open access · bronzeAbstract readReview
In one paragraph

Review in Genes, brain, and behavior, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. AlteredeNeuro · 2026
    Article
  5. Review
  6. AlteredbioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Functional Validation of Alcohol Dependence-AssociatedInternational journal of stem cells · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Substance abuse and neurotransmission.Advances in pharmacology (San Diego, Calif.) · 2022
    Article
  16. Alcohol and the brain: from genes to circuits.Trends in neurosciences · 2021
    Review
  17. Article
  18. Article
  19. cAMP-Fyn signaling in the dorsomedial striatum direct pathway drives excessive alcohol use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  20. Synaptic Plasticity and its Modulation by Alcohol.Brain plasticity (Amsterdam, Netherlands) · 2020
    Review
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

2 authors at 1 institution in 1 country.

N MorisotDepartment of Neurology, University of California, San Francisco, San Francisco, CA, USA.
D RonDepartment of Neurology, University of California, San Francisco, San Francisco, CA, USA.
University of California, San Francisco · US

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2008 to 2017
$13.9M
Pathway-specific Fyn signaling in the striatum and ethanol drinkingU01AA023489 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2014 to 2018
$1.8M
NIAAA NIH HHS P50 AA017072NIAAA NIH HHS U01 AA023489
6 · The paper itself

Abstract

Phenotypes such as motivation to consume alcohol, goal-directed alcohol seeking and habit formation take part in mechanisms underlying heavy alcohol use. Learning and memory processes greatly contribute to the establishment and maintenance of these behavioral phenotypes. The N-methyl-d-aspartate receptor (NMDAR) is a driving force of synaptic plasticity, a key cellular hallmark of learning and memory. Here, we describe data in rodents and humans linking signaling molecules that center around the NMDARs, and behaviors associated with the development and/or maintenance of alcohol use disorder (AUD). Specifically, we show that enzymes that participate in the regulation of NMDAR function including Fyn kinase as well as signaling cascades downstream of NMDAR including calcium/calmodulin-dependent protein kinase II (CamKII), the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and the mammalian target of rapamycin complex 1 (mTORC1) play a major role in mechanisms underlying alcohol drinking behaviors. Finally, we emphasize the brain region specificity of alcohol's actions on the above-mentioned signaling pathways and attempt to bridge the gap between the molecular signaling that drive learning and memory processes and alcohol-dependent behavioral phenotypes. Finally, we present data to suggest that genes related to NMDAR signaling may be AUD risk factors.

Indexed as

Adaptation, PhysiologicalAlcohol-Related DisordersAnimalsHumansMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesReceptors, N-Methyl-D-AspartateSignal TransductionTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesReceptors, N-Methyl-D-AspartateTOR Serine-Threonine KinasesAddictionalcoholAMPAamygdalaCaMKIIFynkinasemTORNMDAnucleus accumbensphosphatasePTPalphasignalingSTEPstriatum

Identifiers

PMID27906494
PMCPMC5444330
OpenAlexW2558817386

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.