Evidence map›Paper›PMID 29329382›Full record

ArticleThe international journal of neuropsychopharmacology2018

Adolescent Synthetic Cannabinoid Exposure Produces Enduring Changes in Dopamine Neuron Activity in a Rodent Model of Schizophrenia Susceptibility.

David D Aguilar, Andrea Giuffrida, Daniel J Lodge

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. GL-II-73, a Positive Allosteric Modulator of α5GABAInternational journal of molecular sciences · 2023
    Article
  5. Article
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  8. Review
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  13. Article
  14. ΔFrontiers in behavioral neuroscience · 2019
    Article
  15. 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

3 authors at 1 institution in 1 country.

David D AguilarDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, Texas.
Andrea GiuffridaDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, Texas.
Daniel J LodgeDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, Texas.
The University of Texas Health Science Center at San Antonio · US

Funding

Stuart T. Hauser Research Training Program in Biological and Social Psychiatry.T32MH016259 · NIMH · JUDGE BAKER CHILDREN'S CENTER · PI Marek Kubicki, Martha E. Shenton · 1985 to 2026
$8.4M
Regulation of ventral hippocampal system functionR01MH090067 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LODGE, DANIEL · 2010 to 2019
$3.5M
Endocannabinoid transmission in schizophreniaR01MH091130 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GIUFFRIDA, ANDREA · 2011 to 2015
$1.9M
Adolescent cannabinoid exposure in a rodent model of schizophrenia susceptibilityF31MH105166 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AGUILAR, DAVID DOMINGUEZ · 2015 to 2016
$31k
NIMH NIH HHS F31 MH105166NIMH NIH HHS R01 MH090067NIMH NIH HHS R01 MH091130NIMH NIH HHS T32 MH016259
6 · The paper itself

Abstract

Background: Epidemiological studies recognize cannabis intake as a risk factor for schizophrenia, yet the majority of adolescents who use marijuana do not develop psychosis. Similarly, the abuse of synthetic cannabinoids poses a risk for psychosis. For these reasons, it is imperative to understand the effects of adolescent cannabinoid exposure in susceptible individuals. Methods: We recently developed a novel rodent model of schizophrenia susceptibility, the F2 methylazoxymethanol acetate rat, where only a proportion (~40%) of rats display a schizophrenia-like phenotype. Using this model, we examined the effects of adolescent synthetic cannabinoid exposure (0.2 mg/kg WIN55, 212-2, i.p.) or adolescent endocannabinoid upregulation (0.3 mg/kg URB597, i.p.) on dopamine neuron activity and amphetamine sensitivity in adulthood. Results: Adolescent synthetic cannabinoid exposure significantly increased the proportion of susceptible rats displaying a schizophrenia-like hyperdopaminergic phenotype after puberty without producing any observable alterations in control rats. Furthermore, this acquired phenotype appears to correspond with alterations in parvalbumin interneuron function within the hippocampus. Endocannabinoid upregulation during adolescence also increased the proportion of susceptible rats developing an increase in dopamine neuron activity; however, it did not alter the behavioral response to amphetamine, further emphasizing differences between exogenous and endogenous cannabinoids. Conclusions: Taken together, these studies provide experimental evidence that adolescent synthetic cannabinoid exposure may contribute to psychosis in susceptible individuals.

Indexed as

Age FactorsAmphetamineAnimalsBehavior, AnimalCannabinoidsCentral Nervous System StimulantsDisease Models, AnimalDisease SusceptibilityDopaminergic NeuronsEndocannabinoidsHippocampusInterneuronsRatsRats, Sprague-DawleySchizophreniaUp-RegulationAmphetamineCannabinoidsCentral Nervous System StimulantsEndocannabinoids

Identifiers

PMID29329382
PMCPMC5887672
OpenAlexW2782901562

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.