Evidence map›Paper›PMID 30731135›Full record

ArticleNeuropharmacology2019

Ketamine normalizes binge drinking-induced defects in glutamatergic synaptic transmission and ethanol drinking behavior in female but not male mice.

Nicole A Crowley, Sarah N Magee, Mengyang Feng, Sarah J Jefferson, Christian J Morris, Nigel C Dao, Dakota F Brockway, Bernhard Luscher

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. A new module in the drug development process: preclinical multi-center randomized controlled trial of R-ketamine on alcohol relapse.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Pre- and postsynaptic signatures in the prelimbic cortex associated with "alcohol use disorder" in the rat.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Somatostatin neurons control an alcohol binge drinking prelimbic microcircuit in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  20. Increased Synaptic Strength and mGluAlcoholism, clinical and experimental research · 2021
    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

8 authors at 1 institution in 1 country.

Nicole A CrowleyDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA; Center for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Sarah N MageeDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA.
Mengyang FengDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA; Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, PA, 16802, USA; Center for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Sarah J JeffersonDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA; Center for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Christian J MorrisDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA; Center for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Nigel C DaoCenter for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA; Department of Biobehavioral Health, Pennsylvania State University, University Park, PA, 16802, USA.
Dakota F BrockwayDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA; Center for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Bernhard LuscherDepartment of Biology, Pennsylvania State University, University Park, PA, 16802, USA; Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, PA, 16802, USA; Center for Molecular Investigation of Neurological Disorders (CMIND), The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA, 16802, USA. Electronic address: BXL25@psu.edu.
Pennsylvania State University · US

Funding

GABAergic Control of Depression Related Brain StatesR01MH099851 · NIMH · PENNSYLVANIA STATE UNIVERSITY, THE · PI LUSCHER, BERNHARD · 2013 to 2019
$3.2M
NIMH NIH HHS R01 MH099851
6 · The paper itself

Abstract

Ketamine is a fast acting experimental antidepressant with significant therapeutic potential for emotional disorders such as major depressive disorder and alcohol use disorders. Of particular interest is binge alcohol use, which during intermittent withdrawal from drinking involves depressive-like symptoms reminiscent of major depressive disorder. Binge drinking has been successfully modeled in mice with the Drinking in the Dark (DID) paradigm, which involves daily access to 20% ethanol, for a limited duration and selectively during the dark phase of the circadian light cycle. Here we demonstrate that DID exposure reduces the cell surface expression of NMDA- and AMPA-type glutamate receptors in the prelimbic cortex (PLC) of female but not male mice, along with reduced activity of the mammalian target of rapamycin (mTOR) signaling pathway. Pretreatment with an acute subanesthetic dose of ketamine suppresses binge-like ethanol consumption in female but not male mice. Lastly, DID-exposure reduces spontaneous glutamatergic synaptic transmission in the PLC of both sexes, but synaptic transmission is rescued by ketamine selectively in female mice. Thus, ketamine may have therapeutic potential as an ethanol binge suppressing agent selectively in female subjects.

Indexed as

AnimalsBinge DrinkingBrainElongation Factor 2 KinaseExcitatory Postsynaptic PotentialsFemaleGlutamic AcidKetamineMaleMiceMice, Inbred C57BLModels, AnimalPrefrontal CortexReceptors, GlutamateSignal TransductionSynaptic TransmissionEef2k protein, mouseElongation Factor 2 KinaseGlutamic AcidKetamineReceptors, GlutamateTOR Serine-Threonine KinasesAlcoholDrinking in the darkKetaminePrelimbic cortex

Identifiers

PMID30731135
PMCPMC6420859
OpenAlexW2911406916

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.