Evidence map›Paper›PMID 36868221›Full record

ArticleNeuron2023

Molecular and cellular mechanisms of the first social relationship: A conserved role of 5-HT from mice to monkeys, upstream of oxytocin.

Yan Liu, Liang Shan, Tiane Liu, Juan Li, Yongchang Chen, Changhong Sun, Chaojuan Yang, Xiling Bian, Yuyu Niu, Chen Zhang and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Neuron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Yan LiuChinese Institutes for Medical Research (CIMR) and Department of Neurobiology, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 10069, China. Electronic address: liuyan@ccmu.edu.cn.
Liang ShanPKU-IDG/McGovern Institute for Brain Research, Peking-Tsinghua Center for Life Sciences, School of Life Sciences, School of Pharmaceutical Sciences, School of Chemistry and Chemical Engineering, Peking University, Beijing 100871, China; Chinese Institute for Brain Research, Beijing, Zhongguangcun Life Science Park, Beijing, China.
Tiane LiuPKU-IDG/McGovern Institute for Brain Research, Peking-Tsinghua Center for Life Sciences, School of Life Sciences, School of Pharmaceutical Sciences, School of Chemistry and Chemical Engineering, Peking University, Beijing 100871, China; Chinese Institute for Brain Research, Beijing, Zhongguangcun Life Science Park, Beijing, China.
Juan LiState Key Laboratory of Natural and Biomimetic Drugs, Department of Biomedical Engineering, College of Engineering, Peking University, Beijing 100871, China.
Yongchang ChenState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, China.
Changhong SunState Key Laboratory of Natural and Biomimetic Drugs, Department of Biomedical Engineering, College of Engineering, Peking University, Beijing 100871, China.
Chaojuan YangChinese Institutes for Medical Research (CIMR) and Department of Neurobiology, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 10069, China.
Xiling BianPKU-IDG/McGovern Institute for Brain Research, Peking-Tsinghua Center for Life Sciences, School of Life Sciences, School of Pharmaceutical Sciences, School of Chemistry and Chemical Engineering, Peking University, Beijing 100871, China; Chinese Institute for Brain Research, Beijing, Zhongguangcun Life Science Park, Beijing, China.
Yuyu NiuState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, China.
Chen ZhangChinese Institutes for Medical Research (CIMR) and Department of Neurobiology, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 10069, China.
Jianzhong XiState Key Laboratory of Natural and Biomimetic Drugs, Department of Biomedical Engineering, College of Engineering, Peking University, Beijing 100871, China.
Yi RaoChinese Institutes for Medical Research (CIMR) and Department of Neurobiology, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 10069, China; PKU-IDG/McGovern Institute for Brain Research, Peking-Tsinghua Center for Life Sciences, School of Life Sciences, School of Pharmaceutical Sciences, School of Chemistry and Chemical Engineering, Peking University, Beijing 100871, China; Changping Laboratory, Yard 28, Science Park Road, Changping District, Beijing, China; Chinese Institute for Brain Research, Beijing, Zhongguangcun Life Science Park, Beijing, China; Research Unit of Medical Neurobiology, Chinese Academy of Medical Sciences, Beijing, China. Electronic address: yrao@pku.edu.cn.
Peking University · CNCapital Medical University · CNKunming University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal affiliation by infants is the first social behavior of mammalian animals. We report here that elimination of the Tph2 gene essential for serotonin synthesis in the brain reduced affiliation in mice, rats, and monkeys. Calcium imaging and c-fos immunostaining showed maternal odors activation of serotonergic neurons in the raphe nuclei (RNs) and oxytocinergic neurons in the paraventricular nucleus (PVN). Genetic elimination of oxytocin (OXT) or its receptor reduced maternal preference. OXT rescued maternal preference in mouse and monkey infants lacking serotonin. Tph2 elimination from RN serotonergic neurons innervating PVN reduced maternal preference. Reduced maternal preference after inhibiting serotonergic neurons was rescued by oxytocinergic neuronal activation. Our genetic studies reveal a role for serotonin in affiliation conserved from mice and rats to monkeys, while electrophysiological, pharmacological, chemogenetic, and optogenetic studies uncover OXT downstream of serotonin. We suggest serotonin as the master regulator upstream of neuropeptides in mammalian social behaviors.

Indexed as

OxytocinSerotoninAnimalsInterpersonal RelationsMammalsMiceParaventricular Hypothalamic NucleusRatsSerotonergic NeuronsOxytocinSerotonin5-HTmaternal affiliation by infantsoxytocinserotoninsocial behavior

Identifiers

PMID36868221
OpenAlexW4322767145

What OpenQuestion holds

Textmetadata
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.