Evidence map›Paper›PMID 42248888›Full record

ArticleNature communications2026

Neuroligin1 in CCK-interneurons gates social memory formation via a disinhibitory microcircuit in the hippocampal CA2 in male mice.

Miao Wu, Zixu Wang, Kun Cao, Chengyan Zhu, Zixuan Wang, Meng Li, Qiaoyun Ren, Ziyue Yi, Xiaojing Yang, Su Wang and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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

13 authors.

Miao Wu *The Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Zixu WangThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Kun CaoThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Chengyan ZhuThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Zixuan WangThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Meng LiThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Qiaoyun RenThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Ziyue YiThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.ORCID http://orcid.org/0000-0003-4816-9270
Xiaojing YangThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Su WangThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.ORCID http://orcid.org/0000-0002-3167-6420
Nannan ChenThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China.
Wei XieThe Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China. wei.xie@seu.edu.cn.ORCID http://orcid.org/0000-0002-9179-4787
An Liu *The Key Laboratory of Developmental Genes and Human Disease, The School of Life Science and Technology, Southeast University, Nanjing, China. liu_an@seu.edu.cn.ORCID http://orcid.org/0000-0003-0421-8050

Funding

Basic Research Program of Jiangsu Province BK20251318National Natural Science Foundation of China (National Science Foundation of China) 32500874National Natural Science Foundation of China (National Science Foundation of China) 32571220National Natural Science Foundation of China (National Science Foundation of China) 91632201
6 · The paper itself

Abstract

Social memory is essential for daily life, and its impairment is associated with psychiatric disorders. The dorsal CA2 (dCA2) region of the hippocampus is known to support social memory formation, yet how it processes social information remains unclear. Here we show that, in male mice, a specific group of dCA2 neurons-cholecystokinin-positive interneurons (CCK-INs)-acts as a hub that receives social cues and activates dCA2 pyramidal neurons (PyNs). Upon social encounters, CCK-INs are activated and suppress parvalbumin-positive interneurons (PV-INs) via GABA

Indexed as

CholecystokininHippocampusInterneuronsMemoryNeuroliginsSocial BehaviorAnimalsCell Adhesion Molecules, NeuronalMaleMiceMice, Inbred C57BLParvalbuminsPyramidal CellsReceptors, GABA-BCell Adhesion Molecules, NeuronalCholecystokininneuroligin 1NeuroliginsParvalbuminsReceptors, GABA-B

Identifiers

PMID42248888
PMCPMC13396340

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.