Evidence map›Paper›PMID 42759179›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026

Genetic and pharmacological evidence linking CB1R signaling to hippocampal GABAergic dysfunction in ASD mouse model.

Jingyi Hu, Haoran Wang, Junyu Ren, Tianyu Liu, Yi Jiang, Yilin Zhang, Yuting Zhang, Han Zhang, Caihong Sun, Mingyang Zou

Abstract read
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In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Jingyi HuDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Haoran WangDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Junyu RenDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Tianyu LiuDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Yi JiangDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Yilin ZhangDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China; Yunnan Institute of Endemic Diseases Control and Prevention (YIEDC), Kunming, China.
Yuting ZhangDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Han ZhangDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China.
Caihong SunDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China; Department of Developmental Behavioral Pediatrics, the Sixth Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address: 200033@hrbmu.edu.cn.
Mingyang ZouDepartment of Children's and Adolescent Health, School of Public Health, Harbin Medical University, Harbin, China; Heilongjiang Province Key Laboratory of Child Development and Genetic Research, Harbin Medical University, Harbin, China. Electronic address: mingyangshine@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder increasingly linked to disrupted GABAergic inhibition and altered excitatory-inhibitory balance. Cannabinoid receptor 1 (CB1R), enriched on GABAergic interneurons, modulates inhibitory tone. Whether CB1R dysfunction in GABAergic neurons contributes to ASD-like phenotypes remains unclear. This study investigated the role of CB1R in GABAergic regulation and evaluated whether pharmacological CB1R activation could ameliorate GABAergic abnormalities and behavioral deficits in ASD models. We generated conditional CB1R knockout mice in GABAergic neurons (GABA-CB1

Indexed as

Autism spectrum disorder (ASD)CB1RConditional knockoutGABAergic systemSynaptic dysfunction

Identifiers

PMID42759179
PMCPMC13602063

What OpenQuestion holds

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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.