Evidence map›Paper›PMID 34589838›Full record

ArticleBrain, behavior, & immunity - health2020

Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia.

Max W Katz-Barber, Sharon L Hollins, Annalisa Cuskelly, Angeline J W Leong, Ariel Dunn, Lauren Harms, Deborah M Hodgson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain, behavior, & immunity - health, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 12% 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, 16 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Max W Katz-BarberLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Sharon L HollinsLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Annalisa CuskellyLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Angeline J W LeongLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Ariel DunnLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Lauren HarmsLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Deborah M HodgsonLaboratory of Neuroimmunology, School of Psychology, University of Newcastle, Callaghan, NSW, Australia.
Hunter Medical Research Institute · AUUniversity of Newcastle Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough the aetiology of schizophrenia remains unknown, it has been suggested that it might occur in response to alterations in the gut-brain axis (GBA), the bi-directional communication system between the gut and the brain. The current study aimed to determine whether the "two-hit" animal model of neuropsychopathology (maternal immune activation combined with adolescent cannabinoid exposure), produced abnormalities in the GBA.

methodPregnant Wistar rats were administered the viral mimetic polyI:C on gestational day 19 and offspring were administered the synthetic cannabinoid HU210 from postnatal days 35-48. Evidence of GBA activation was assessed in the hypothalamus, colon and fecal samples from male and female offspring at adolescence and adulthood.

resultsFindings were sex-specific with adolescent female offspring exhibiting an increased hypothalamic inflammatory profile, increased hypothalamic CRHR1 mRNA, and decreased fecal expression of

conclusionThese results indicate that the rat two-hit model, documented to produce behavioural and neuroanatomical abnormalities, also produces hypothalamic and microbiota abnormalities. The results also demonstrate significant sex differences, suggesting that this model may be useful for investigating the role of the GBA in the aetiology of neurodevelopmental disorders such as schizophrenia.

Indexed as

Adolescent cannabisGut-brain axisHPA axisMicrobiomeNeuropsychiatric disordersPrenatal infectionSchizophrenia

Identifiers

PMID34589838
PMCPMC8474551
OpenAlexW3006510648

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.