Evidence map›Paper›PMID 35840800›Full record

ArticleMolecular psychiatry2022

A short period of early life oxytocin treatment rescues social behavior dysfunction via suppression of hippocampal hyperactivity in male mice.

Libiao Pan, Lu Zheng, Xiaotong Wu, Zhenggang Zhu, Siyu Wang, Yi Lu, Yang He, Qian Yang, Xiaolin Ma, Xiaomeng Wang and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Lasting effects of early-life oxytocin treatment on LTP and episodic memory in a mouse model of Fragile X syndrome.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  6. Review
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  11. Review
  12. Review
  13. Pharmacological reduction of reverse-translated hippocampal hyperactivity in mouse: relevance for psychosis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  14. N-acetyl cysteine through modulation of HDACIBRO neuroscience reports · 2025
    Article
  15. Article
  16. Article
  17. How does oxytocin modulate human behavior?Molecular psychiatry · 2025
    Review
  18. Article
  19. Article
  20. 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

20 authors at 3 institutions in 2 countries.

Libiao Pan *Department of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Lu Zheng *Department of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Xiaotong Wu *Department of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Zhenggang ZhuDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Siyu WangDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Yi LuDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Yang HeDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Qian YangDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Xiaolin MaDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Xiaomeng WangDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Hongbin YangDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Li ZhanDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Yujian LuoDepartment of Neurology of the First Affiliated Hospital, Interdisciplinary Institute of Neuroscience and Technology, Zhejiang University School of Medicine, Hangzhou, 310027, China.
Xiangyao LiDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.ORCID http://orcid.org/0000-0002-4793-0550
Yudong ZhouDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.ORCID http://orcid.org/0000-0002-6364-3869
Xiaodong WangDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.ORCID http://orcid.org/0000-0001-7730-3710
Jianhong LuoDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Lang WangDepartment of Neurology of the First Affiliated Hospital, Interdisciplinary Institute of Neuroscience and Technology, Zhejiang University School of Medicine, Hangzhou, 310027, China.
Shumin DuanDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.ORCID http://orcid.org/0000-0002-0466-1821
Hao WangDepartment of Neurobiology and Department of Neurosurgery of Second Affiliated Hospital, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China. haowang@zju.edu.cn.ORCID http://orcid.org/0000-0003-1862-8229
Zhejiang Lab · CNZhejiang University · CNAllen Institute for Brain Science · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early sensory experiences interact with genes to shape precise neural circuits during development. This process is vital for proper brain function in adulthood. Neurological dysfunctions caused by environmental alterations and/or genetic mutation may share the same molecular or cellular mechanisms. Here, we show that early life bilateral whisker trimming (BWT) subsequently affects social discrimination in adult male mice. Enhanced activation of the hippocampal dorsal CA3 (dCA3) in BWT mice was observed during social preference tests. Optogenetic activation of dCA3 in naive mice impaired social discrimination, whereas chemogenetic silencing of dCA3 rescued social discrimination deficit in BWT mice. Hippocampal oxytocin (OXT) is reduced after whisker trimming. Neonatal intraventricular compensation of OXT relieved dCA3 over-activation and prevented social dysfunction. Neonatal knockdown of OXT receptor in dCA3 mimics the effects of BWT, and cannot be rescued by OXT treatment. Social behavior deficits in a fragile X syndrome mouse model (Fmr1 KO mice) could also be recovered by early life OXT treatment, through negating dCA3 over-activation. Here, a possible avenue to prevent social dysfunction is uncovered.

Indexed as

Fragile X SyndromeOxytocinAnimalsFragile X Messenger Ribonucleoprotein 1HippocampusMaleMiceReceptors, OxytocinSocial BehaviorFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1OxytocinReceptors, Oxytocin

Identifiers

PMID35840800
PMCPMC9718675
OpenAlexW4285493621

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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.