Evidence map›Paper›PMID 42321470›Full record

ArticleNature neuroscience2026

Tryptamine from wake-active monoaminergic neurons regulates sleep homeostasis.

Huateng Cao, Kui Wang, Jin Zhao, Zhong-Hua Zha, Qian Zhang, Yijin Xiu, Bangsheng Wu, Shajin Huang, Xiao-Na Zhu, Xiaoting Li and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 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

22 authors.

Huateng CaoInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.ORCID http://orcid.org/0000-0001-9622-3812
Kui WangInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Jin ZhaoInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Zhong-Hua ZhaiHuman Institute, ShanghaiTech University, Shanghai, China.
Qian ZhangInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Yijin XiuInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Bangsheng WuDepartment of Neurology and National Center for Neurological Diseases, Huashan Hospital, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.
Shajin HuangInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Xiao-Na ZhuShanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, National Center for Mental Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University, School of Medicine and School of Psychology, Shanghai, China.
Xiaoting LiiHuman Institute, ShanghaiTech University, Shanghai, China.
Jianan ChenDP Technology, Beijing, China.
Han WenAI for Science Institute, Beijing, China.
Siwen PanInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Ke-Xin YangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Ji HuSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.ORCID http://orcid.org/0000-0001-7930-2316
Jin-Tai YuDepartment of Neurology and National Center for Neurological Diseases, Huashan Hospital, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-2532-383X
Zhi-Jie LiuiHuman Institute, ShanghaiTech University, Shanghai, China.ORCID http://orcid.org/0000-0001-7279-2893
Tian HuaiHuman Institute, ShanghaiTech University, Shanghai, China.
Yu MuInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China. my@ion.ac.cn.ORCID http://orcid.org/0000-0001-9297-4854
Zhian HuDepartment of Physiology, Institute of Brain and Intelligence, Third Military Medical University, Chongqing, China. zhianhu@aliyun.com.ORCID http://orcid.org/0000-0002-4439-537X
Peng YuanDepartment of Rehabilitation Medicine, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Institute for Translational Brain Research, MOE Frontiers Center for Brain Science, MOE Innovative Center for New Drug Development of Immune Inflammatory Diseases, Fudan University, Shanghai, China. pyuan@fudan.edu.cn.ORCID http://orcid.org/0000-0003-4051-4447
Zhe ZhangInstitute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China. zhezhang@ion.ac.cn.ORCID http://orcid.org/0000-0002-0899-8077

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32100799National Natural Science Foundation of China (National Science Foundation of China) U23A20433
6 · The paper itself

Abstract

Wakefulness produces sleep-promoting substances and the cerebrospinal fluid contains substances that reflect homeostatic sleep pressure. However, identities of such molecules, and the neural mechanisms for producing and sensing them, remain mysterious. Here we show that cerebrospinal fluid levels of tryptamine (TrpA) track homeostatic sleep pressure in nocturnal mice and diurnal pigs, reflecting physical activity history independently of light-dark cycles. We developed a ratiometric fluorescent sensor for TrpA and showed that TrpA is produced by wake-active monoaminergic nuclei in the diencephalon and brainstem and is secreted in an activity-dependent manner. We showed that released TrpA binds to G-protein-coupled receptor 139 (GPR139) and enhances neuronal excitability in the hypothalamic preoptic area to promote sleep. TrpA-GPR139 signaling was necessary for homeostatic sleep rebound and small-molecule GPR139 agonists promoted sleep duration and quality. Together, our study reveals TrpA as a signal related to sleep homeostasis and GPR139 as a druggable target against its disruption.

Indexed as

Biogenic MonoaminesHomeostasisNeuronsSleepTryptaminesWakefulnessAnimalsMaleMiceMice, Inbred C57BLReceptors, G-Protein-CoupledSwineBiogenic MonoaminesReceptors, G-Protein-CoupledtryptamineTryptamines

Identifiers

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.