Evidence map›Paper›PMID 37584417›Full record

SynthesisSchizophrenia bulletin2024

Prefrontal and Hippocampal Parvalbumin Interneurons in Animal Models for Schizophrenia: A Systematic Review and Meta-analysis.

Thamyris Santos-Silva, Débora Dos Santos Fabris, Cilene Lino de Oliveira, Francisco S Guimarães, Felipe V Gomes

Open access · greenAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Schizophrenia bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  8. Review
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  10. Review
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  12. Multi-level therapeutic actions of cannabidiol in ketamine-induced schizophrenia psychopathology in male rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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  14. 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

5 authors at 1 institution in 1 country.

Thamyris Santos-SilvaDepartment of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0001-5129-5695
Débora Dos Santos FabrisDepartment of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Cilene Lino de OliveiraDepartment of Physiological Sciences, Center of Biological Sciences, University of Santa Catarina, Florianópolis,Brazil.
Francisco S GuimarãesDepartment of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Felipe V GomesDepartment of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0003-1033-1850
Universidade de São Paulo · BR

Funding

Alexander von Humboldt FoundationCoordination for the Improvement of Higher Education Personnel-Brazil #88887.334572/2019-00São Paulo Research Foundation 19/24591-4
6 · The paper itself

Abstract

backgroundConsistent with postmortem findings in patients, most animal models for schizophrenia (SCZ) present abnormal levels of parvalbumin (PV), a marker of fast-spiking GABAergic interneurons, in the prefrontal cortex (PFC) and hippocampus (HIP). However, there are discrepancies in the literature. PV reductions lead to a functional loss of PV interneurons, which is proposed to underly SCZ symptoms. Given its complex etiology, different categories of animal models have been developed to study SCZ, which may distinctly impact PV levels in rodent brain areas. STUDY

designWe performed a quantitative meta-analysis on PV-positive cell number/density and expression levels in the PFC and HIP of animal models for SCZ based on pharmacological, neurodevelopmental, and genetic manipulations.

resultsOur results confirmed that PV levels are significantly reduced in the PFC and HIP regardless of the animal model. By categorizing into subgroups, we found that all pharmacological models based on NMDA receptor antagonism decreased PV-positive cell number/density or PV expression levels in both brain areas examined. In neurodevelopmental models, abnormal PV levels were confirmed in both brain areas in maternal immune activation models and HIP of the methylazoxymethanol acetate model. In genetic models, negative effects were found in neuregulin 1 and ERBB4 mutant mice in both brain regions and the PFC of dysbindin mutant mice. Regarding sex differences, male rodents exhibited PV reductions in both brain regions only in pharmacological models, while few studies have been conducted in females.

conclusionOverall, our findings support deficits in prefrontal and hippocampal PV interneurons in animal models for SCZ.

Indexed as

SchizophreniaAnimalsDisease Models, AnimalFemaleHippocampusHumansInterneuronsMaleMiceParvalbuminsPrefrontal CortexParvalbuminsexcitatory-inhibitory balanceGABA/preclinical researchmodel organismspsychiatrypsychosis

Identifiers

PMID37584417
PMCPMC10754178
OpenAlexW4385850698

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.