Evidence map›Paper›PMID 42501224›Full record

ArticleNeuroscience bulletin2026

Nucleus Accumbens D1 Receptor Neurons Contribute to Emotional and Metabolic Adaptation to Chronic Hypoxia.

Yan Chen, Jie Shao, Lu Zhang, Yuchuan Hong, Hao Yang, Shirui Jun, William Weijia Lu, Jie Tu, Guoxin Ni, Fan Yang

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Article in Neuroscience bulletin, 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

10 authors.

Yan Chen *The Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Jie Shao *The Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Lu ZhangThe Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Yuchuan HongThe Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Hao YangState Key Laboratory of Genetic Engineering, Human Phenome Institute, School of Life Sciences and Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, 200433, China.
Shirui JunThe Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
William Weijia LuFaculty of Pharmaceutical Sciences, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Jie TuThe Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China. jie.tu@siat.ac.cn.
Guoxin NiDepartment of Rehabilitation Medicine, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China. nigx@xmu.edu.cn.
Fan YangThe Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China. fan.yang@siat.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hypoxia at high altitudes disrupts emotional and metabolic homeostasis. However, the underlying mechanisms remain unclear. Using mice chronically exposed to 11.35% oxygen, we combined three-dimensional motion capture, anxiety-related behavioral tests, brain-wide c-Fos mapping, and metabolic cage recordings. Hypoxic mice showed anxiety-like behavior, altered posture, and spontaneous behavioral distribution, elevated oxygen consumption, carbon dioxide production, and energy expenditure, together with reduced feeding. c-Fos mapping implicated the limbic, prefrontal, hypothalamic, and nucleus accumbens shell (NAcSh) regions in hypoxic adaptation. Selective depolarization of NAcSh dopamine D1 receptor (D1R) neurons alleviated anxiety-like behavior and attenuated hypoxia-associated hypermetabolism while further shifting substrate utilization. Exercise preconditioning also reduced anxiety-like behavior and partially restored NAcSh D1R-related signaling. Together, these findings identify NAcSh D1R-related signaling as a key component of chronic hypoxia adaptation and show that activation of NAcSh D1R neurons is sufficient to attenuate the coupled anxiety-like and metabolic phenotypes.

Indexed as

Anxiety-like behaviorChronic hypoxiaDopamine D1 receptorExercise preconditioningMetabolic phenotypingNucleus accumbens shellThree-dimensional motion capture

Identifiers

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Registered trials

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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.