Evidence map›Paper›PMID 25445065›Full record

ArticleProgress in neuro-psychopharmacology & biological psychiatry2015

Behavioral alterations in rat offspring following maternal immune activation and ELR-CXC chemokine receptor antagonism during pregnancy: implications for neurodevelopmental psychiatric disorders.

Stephanie A Ballendine, Quentin Greba, Wojciech Dawicki, Xiaobei Zhang, John R Gordon, John G Howland

Abstract read
In one paragraph

Article in Progress in neuro-psychopharmacology & biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

28 citing papers in PubMed, 70 citations in OpenAlex.

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  16. Review
  17. Maternal immune activation: reporting guidelines to improve the rigor, reproducibility, and transparency of the model.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    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

6 authors at 1 institution in 1 country.

Stephanie A BallendineDept. of Physiology, University of Saskatchewan, GB33, Health Sciences Building, 107 Wiggins Rd, Saskatoon, SK S7N5E5, Canada.
Quentin GrebaDept. of Physiology, University of Saskatchewan, GB33, Health Sciences Building, 107 Wiggins Rd, Saskatoon, SK S7N5E5, Canada.
Wojciech DawickiDept. of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Xiaobei ZhangDept. of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
John R GordonDept. of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
John G HowlandDept. of Physiology, University of Saskatchewan, GB33, Health Sciences Building, 107 Wiggins Rd, Saskatoon, SK S7N5E5, Canada. Electronic address: john.howland@usask.ca.
University of Saskatchewan · CA

Funding

CIHR 118032-1CIHR 125984CIHR 125984-1
6 · The paper itself

Abstract

Research suggests that maternal immune activation (MIA) during pregnancy increases the risk of neurodevelopmental disorders including schizophrenia and autism in the offspring. Current theories suggest that inflammatory mediators including cytokines and chemokines may underlie the increased risk of these disorders in humans. For example, elevated maternal interleukin-8 (IL-8) during pregnancy is associated with increased risk of schizophrenia in the offspring. Given this association, the present experiments examined ELR-CXC chemokines CXCL1 and CXCL2, rodent homologues of human IL-8, and activation of their receptors (CXCR1 and CXCR2) in an established rodent model of MIA. Pregnant Long Evans rats were treated with the viral mimetic polyinosinic-polycytidylic acid (polyI:C; 4 mg/kg, i.v.) on gestational day 15. Protein analysis using multiplex assays and ELISA showed that polyI:C significantly increased maternal serum concentrations of interleukin-1β, tumor necrosis factor, and CXCL1 3h after administration. Subsequent experiments tested the role of elevated maternal CXCL1 on behavior of the offspring by administering a CXCR1/CXCR2 antagonist (G31P; 500 μg/kg, i.p.; 1h before, 48 and 96 h after polyI:C treatment). The male offspring of dams treated with polyI:C demonstrated subtle impairments in prepulse inhibition (PPI), impaired associative and crossmodal recognition memory, and altered behavioral flexibility in an operant test battery. While G31P did not completely reverse the behavioral impairments caused by polyI:C, it enhanced PPI during adolescence and strategy set-shifting and reversal learning during young adulthood. These results suggest that while polyI:C treatment significantly increases maternal CXCL1, elevations of this chemokine are not solely responsible for the effects of polyI:C on the behavior of the offspring.

Indexed as

AnimalsBehavior, AnimalChemokine CXCL1Chemokine CXCL2Conditioning, OperantCuesFemaleInterleukin-8MaleMental DisordersPeptide FragmentsPoly I-CPregnancyPregnancy, AnimalPrenatal Exposure Delayed EffectsPrepulse InhibitionChemokine CXCL1Chemokine CXCL2CXCL8(3-73)K11R,G31P, bovineInterleukin-8Peptide FragmentsPoly I-CReceptors, CXCRReceptors, Interleukin-8AReceptors, Interleukin-8BCrossmodal memoryInterleukin-8Polyi:CSchizophreniaSet-shifting

Identifiers

PMID25445065
PMCPMC4464825
OpenAlexW1965456396

What OpenQuestion holds

Textmetadata
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.