Evidence map›Paper›PMID 27186643›Full record

ArticlePloS one2016

Impaired Ethanol-Induced Sensitization and Decreased Cannabinoid Receptor-1 in a Model of Posttraumatic Stress Disorder.

Jessica J Matchynski-Franks, Laura L Susick, Brandy L Schneider, Shane A Perrine, Alana C Conti

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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

5 authors at 3 institutions in 1 country.

Jessica J Matchynski-FranksResearch Service, John D. Dingell VA Medical Center, Detroit, Michigan, United States of America.
Laura L SusickResearch Service, John D. Dingell VA Medical Center, Detroit, Michigan, United States of America.
Brandy L SchneiderResearch Service, John D. Dingell VA Medical Center, Detroit, Michigan, United States of America.
Shane A PerrineDepartment of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan, United States of America.
Alana C ContiResearch Service, John D. Dingell VA Medical Center, Detroit, Michigan, United States of America.
John D. Dingell VA Medical Center · USMichigan United · USWayne State University · US

Funding

Longitudinal Assessment of Cortical Hypoactivity in a Model of Comorbid TBI-PTSDI01RX001511 · VA · JOHN D DINGELL VA MEDICAL CENTER · PI CONTI, ALANA C. · 2015 to 2019
–
RRD VA I01 RX001511
6 · The paper itself

Abstract

background and purposeImpaired striatal neuroplasticity may underlie increased alcoholism documented in those with posttraumatic stress disorder (PTSD). Cannabinoid receptor-1 (CB1) is sensitive to the effects of ethanol (EtOH) and traumatic stress, and is a critical regulator of striatal plasticity. To investigate CB1 involvement in the PTSD-alcohol interaction, this study measured the effects of traumatic stress using a model of PTSD, mouse single-prolonged stress (mSPS), on EtOH-induced locomotor sensitization and striatal CB1 levels.

methodsMice were exposed to mSPS, which includes: 2-h restraint, 10-min group forced swim, 15-min exposure to rat bedding odor, and diethyl ether exposure until unconsciousness or control conditions. Seven days following mSPS exposure, the locomotor sensitizing effects of EtOH were assessed. CB1, post-synaptic density-95 (PSD95), and dopamine-2 receptor (D2) protein levels were then quantified in the dorsal striatum using standard immunoblotting techniques.

resultsMice exposed to mSPS-EtOH demonstrated impaired EtOH-induced locomotor sensitization compared to Control-EtOH mice, which was accompanied by reduced striatal CB1 levels. EtOH increased striatal PSD95 in control and mSPS-exposed mice. Additionally, mSPS-Saline exposure increased striatal PSD95 and decreased D2 protein expression, with mSPS-EtOH exposure alleviating these changes.

conclusionsThese data indicate that the mSPS model of PTSD blunts the behavioral sensitizing effects of EtOH, a response that suggests impaired striatal neuroplasticity. Additionally, this study demonstrates that mice exposed to mSPS and repeated EtOH exposure decreases CB1 in the striatum, providing a mechanism of interest for understanding the effects of EtOH following severe, multimodal stress exposure.

Indexed as

AnimalsCorpus StriatumDisease Models, AnimalDisks Large Homolog 4 ProteinEthanolGuanylate KinasesLocomotionMaleMembrane ProteinsMiceMice, Inbred C57BLReceptor, Cannabinoid, CB1Receptors, Dopamine D2Stress Disorders, Post-TraumaticDisks Large Homolog 4 ProteinDlg4 protein, mouseEthanolGuanylate KinasesMembrane ProteinsReceptor, Cannabinoid, CB1Receptors, Dopamine D2

Identifiers

PMID27186643
PMCPMC4871361
OpenAlexW2402188890

What OpenQuestion holds

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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.