Evidence map›Paper›PMID 25522381›Full record

ArticleThe international journal of neuropsychopharmacology2014

Effects of pubertal cannabinoid administration on attentional set-shifting and dopaminergic hyper-responsivity in a developmental disruption model of schizophrenia.

Felipe V Gomes, Francisco S Guimarães, Anthony A Grace

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Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  10. Animal Models of Relevance to the Schizophrenia Prodrome.Biological psychiatry global open science · 2023
    Review
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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.

Felipe V GomesDepartment of Pharmacology, Medical School of Ribeirão Preto, University of São Paulo, Brazil (Drs Gomes and Guimarães); Center for Interdisciplinary Research on Applied Neurosciences, University of São Paulo, Brazil (Drs Gomes and Guimarães); Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, A210 Langley Hall, Pittsburgh, PA 15260 (Dr Grace). gomesfv@usp.br.
Francisco S GuimarãesDepartment of Pharmacology, Medical School of Ribeirão Preto, University of São Paulo, Brazil (Drs Gomes and Guimarães); Center for Interdisciplinary Research on Applied Neurosciences, University of São Paulo, Brazil (Drs Gomes and Guimarães); Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, A210 Langley Hall, Pittsburgh, PA 15260 (Dr Grace).
Anthony A GraceDepartment of Pharmacology, Medical School of Ribeirão Preto, University of São Paulo, Brazil (Drs Gomes and Guimarães); Center for Interdisciplinary Research on Applied Neurosciences, University of São Paulo, Brazil (Drs Gomes and Guimarães); Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, A210 Langley Hall, Pittsburgh, PA 15260 (Dr Grace).

Funding

Gating of Information Flow Within the Nucleus Accumbens (Supplement)R01MH057440 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ANTHONY A GRACE · 1997 to 2026
$7.2M
Gating of Information Flow Within the Nucleus AccumbensR37MH057440 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRACE, ANTHONY A · 2007 to 2016
$3.3M
NIMH NIH HHS MH57440NIMH NIH HHS R01 MH057440NIMH NIH HHS R37 MH057440
6 · The paper itself

Abstract

backgroundAdolescent exposure to cannabinoids in vulnerable individuals is proposed to be a risk factor for psychiatric conditions later in life, particularly schizophrenia. Evidence from studies in animals has indicated that a combination of repeated pubertal cannabinoid administration with either neonatal prefrontocortical lesion, isolation rearing, or chronic NMDA receptor antagonism administration induces enhanced schizophrenia-like behavioral disruptions. The effects of adolescent exposure to CB1 receptor agonists, however, have not been tested in a developmental disruption model of schizophrenia.

methodsThis was tested in the methylazoxymethanol (MAM) model, in which repeated treatment with the synthetic cannabinoid agonist WIN 55,212-2 (WIN; 1.2mg/kg) was extended over 25 days throughout puberty (postnatal days 40-65) in control and MAM rats. The rats received 20 injections, which were delivered irregularly to mimic the human condition. Adult rats were tested for attentional set-shifting task and locomotor response to amphetamine, which was compared with in vivo recording from ventral tegmental area (VTA) dopamine (DA) neurons.

resultsMAM-treated rats showed impairment in the attentional set-shifting task, augmented locomotor response to amphetamine administration, and an increased number of spontaneously active DA neurons in the VTA. Interestingly, pubertal WIN treatment in normal animals induced similar changes at adulthood as those observed in MAM-treated rats, supporting the notion that adolescence exposure to cannabinoids may represent a risk factor for developing schizophrenia-like signs at adulthood. However, contrary to expectations, pubertal WIN administration did not exacerbate the behavioral and electrophysiological changes in MAM-treated rats beyond that observed in WIN-treated saline rats (Sal). Indeed, WIN treatment actually attenuated the locomotor response to amphetamine in MAM rats without impacting DA neuron activity states.

conclusionsTaken together, the present results indicate that the impact of cannabinoids during puberty/adolescence on schizophrenia models is more complex than may be predicted.

Indexed as

AmphetamineAnimalsAttentionBenzoxazinesCannabinoidsCentral Nervous System StimulantsDisease Models, AnimalDopaminergic NeuronsExecutive FunctionFemaleMaleMethylazoxymethanol AcetateMorpholinesMotor ActivityNaphthalenesNeuropsychological Tests(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanoneAmphetamineBenzoxazinesCannabinoidsCentral Nervous System StimulantsmethylazoxymethanolMethylazoxymethanol AcetateMorpholinesNaphthalenesadolescencecannabinoiddopamineMAM treatmentschizophrenia.

Identifiers

PMID25522381
PMCPMC4368886

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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.