Evidence map›Paper›PMID 40764556›Full record

ArticleBMC biology2025

Ephrin-B2 deletion in GABAergic neurons induces cognitive deficits associated with single-nucleus transcriptomic differences in the prefrontal cortex.

Peijun Ju, Yu Fang, Siying Xiang, Weidi Wang, Ying Sun, Wei Wang, Yanli Ding, Chao Luo, Ping Jiang, Jianhua Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Peijun Ju *Shanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu Fang *Shanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Siying Xiang *Shanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Weidi WangShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ying SunShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wei WangShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yanli DingShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chao LuoShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ping JiangShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China. jiangping413@126.com.
Jianhua ChenShanghai Institute of Traditional Chinese Medicine for Mental Health, Shanghai Key Laboratory of Psychotic Disorders, Shanghai Clinical Research Center for Mental Health, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China. chenjhv@hotmail.com.

Funding

National Natural Science Foundation of China 82071500Open Project Funded by the Shanghai Institute of Traditional Chinese Medicine for Mental Health SZB2023204Project for China Hospital Development Institute, Shanghai Jiao Tong University CHDI-2023-B-19Science Popularization and Innovation Project in Xuhui District, Shanghai xhkp-HM-2024017Shanghai Municipal Administrator of Traditional Chinese Medicine ZY-(2021-2023)-0207-01Shanghai Science and Technology Innovation Program 21Y11921100the Natural Science Foundation of Shanghai, China 23ZR1454600the Program of Shanghai Academic/Technology Research Leader 21XD1423300
6 · The paper itself

Abstract

backgroundEphrin-B2 (EB2) signaling plays a crucial role in regulating memory and synaptic plasticity. Comprehensive identification of cell-type-specific transcriptomic changes in EB2 knockout mice is expected to shed light on potential mechanisms associated with EB2 signaling in cognitive functions.

resultsOur study captures changes in cell populations in response to EB2 manipulation and reveals previously uncharacterized cell types (CPA6 + inhibitory neurons) in the mPFC. We validated the differential transcriptomic activity of Pbx1 and Meis1 in CPA6 + neurons using fluorescence in situ hybridization (ISH) in EB2-vGATCre mice. The aberrant presence of CPA6 + neurons in the mPFC may correlate with cognitive impairments induced by EB2 deletion in vGAT + neurons. Analyzing differentially expressed genes (DEGs) in individual cell clusters, we identified alterations related to synapse organization and development, cognition, amyloid-beta formation, and locomotor behavior. Additionally, our DEGs overlapped with human genome-wide association study (GWAS) candidate genes related to cognition and anxiety, underscoring the relevance of our mouse model to human disease.

conclusionsWe present a comprehensive atlas of cell-type-specific gene expression changes in this synaptic deficiency model and identify novel cell-type-specific targets implicated in cognitive deficits. Our investigation provides a detailed map of the cell types, genes, and pathways altered in this inhibitory synaptic deficiency model.

Indexed as

Cognitive DysfunctionEphrin-B2GABAergic NeuronsGene DeletionPrefrontal CortexTranscriptomeAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutEphrin-B2CognitionEphrin-B2GABAergic neuronsSingle-nucleus RNA sequencing

Identifiers

PMID40764556
PMCPMC12326787

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LicenceCC BY-NC-ND
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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.