Evidence map›Paper›PMID 32718349›Full record

ArticleMolecular autism2020

Targeting PPARα in the rat valproic acid model of autism: focus on social motivational impairment and sex-related differences.

Simona Scheggi, Francesca Guzzi, Giulia Braccagni, Maria Graziella De Montis, Marco Parenti, Carla Gambarana

Abstract read
In one paragraph

Article in Molecular autism, 2020. 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
–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

28 citing papers in PubMed.

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  11. The effect of inhibiting hindbrain A2 noradrenergic neurons by 6-Hydroxydopamine on lipopolysaccharide-treated male rats autistic animal model.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
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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.

Simona ScheggiDepartment Molecular and Developmental Medicine, University of Siena, Via Aldo Moro, 2, Siena, Italy. simona.scheggi@unisi.it.ORCID 0000-0002-0229-6090
Francesca GuzziDepartment Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.
Giulia BraccagniDepartment Molecular and Developmental Medicine, University of Siena, Via Aldo Moro, 2, Siena, Italy.
Maria Graziella De MontisDepartment Molecular and Developmental Medicine, University of Siena, Via Aldo Moro, 2, Siena, Italy.
Marco ParentiDepartment Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.
Carla GambaranaDepartment Molecular and Developmental Medicine, University of Siena, Via Aldo Moro, 2, Siena, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe social motivational theory of autism spectrum disorder (ASD) focuses on social anhedonia as key causal feature of the impaired peer relationships that characterize ASD patients. ASD prevalence is higher in boys, but increasing evidence suggests underdiagnosis and undertreatment in girls. We showed that stress-induced motivational anhedonia is relieved by repeated treatment with fenofibrate (FBR), a peroxisome proliferator-activated receptor α (PPARα) agonist. Here, we used the valproic acid (VPA) model of ASD in rats to examine male and female phenotypes and assess whether FBR administration from weaning to young adulthood relieved social impairments.

methodsMale and female rats exposed to saline or VPA at gestational day 12.5 received standard or FBR-enriched diet from postnatal day 21 to 48-53, when behavioral tests and ex vivo neurochemical analyses were performed. Phosphorylation levels of DARPP-32 in response to social and nonsocial cues, as index of dopamine D

resultsFBR administration relieved social impairment and perseverative behavior in VPA-exposed male and female rats, but it was only effective on female stereotypies. Dopamine D LIMITATIONS: This study did not directly address the extent of motivational deficit in VPA-exposed rats and whether FBR administration restored the likely decreased motivation to operate for social reward. Future studies using operant behavior protocols will address this relevant issue.

conclusionsThe results support the involvement of impaired motivational mechanisms in ASD-like social deficits and suggest the rationale for a possible pharmacological treatment. Moreover, the study highlights sex-related differences in the expression of ASD-like symptoms and their differential responses to FBR treatment.

Indexed as

MotivationSex CharacteristicsSocial BehaviorAnimalsAnxietyAutistic DisorderBehavior, AnimalBiomarkersDisease Models, AnimalFemaleFenofibrateMaleMaze LearningNucleus AccumbensPPAR alphaPregnancyBiomarkersFenofibratePPAR alphaValproic AcidAnimal modelsAutism spectrum disorderDopamineRewardValproic acid

Identifiers

PMID32718349
PMCPMC7385875

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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.