Evidence map›Paper›PMID 36759610›Full record

ArticleNature communications2023

Astrocytic lactate dehydrogenase A regulates neuronal excitability and depressive-like behaviors through lactate homeostasis in mice.

Shan Yao, Min-Dong Xu, Ying Wang, Shen-Ting Zhao, Jin Wang, Gui-Fu Chen, Wen-Bing Chen, Jian Liu, Guo-Bin Huang, Wen-Juan Sun and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
11.1field-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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
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  11. bioRxiv : the preprint server for biology · 2026
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  16. ALS-FTD-linked CCNFJournal of neuroinflammation · 2026
    Article
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23 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 1 country.

Shan Yao *Department of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Min-Dong Xu *Department of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.ORCID 0000-0001-5643-3364
Ying Wang *Department of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Shen-Ting Zhao *Department of Physiology, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Jin WangDepartment of Physiology, Guangxi University of Science and Technology, Liuzhou, 545005, China.
Gui-Fu ChenDepartment of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Wen-Bing ChenInstitute of Life Science, Nanchang University, Nanchang, 330031, China.ORCID 0000-0002-3386-7212
Jian LiuDepartment of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Guo-Bin HuangDepartment of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Wen-Juan SunDepartment of Physiology, Guangxi University of Science and Technology, Liuzhou, 545005, China.
Yan-Yan ZhangDepartment of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Huan-Li HouDepartment of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China.
Lei LiSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.ORCID 0000-0002-9542-4767
Xiang-Dong SunDepartment of Neurology of the Second Affiliated Hospital, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 510260, China. xisun@gzhmu.edu.cn.ORCID 0000-0002-0051-1463
Second Affiliated Hospital of Guangzhou Medical University · CNGuangxi University of Science and Technology · CNGuangzhou Medical University · CNNanchang University · CNShanghaiTech University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in energy metabolism are associated with depression. However, the role of glycolysis in the pathogenesis of depression and the underlying molecular mechanisms remain unexplored. Through an unbiased proteomic screen coupled with biochemical verifications, we show that the levels of glycolysis and lactate dehydrogenase A (LDHA), a glycolytic enzyme that catalyzes L-lactate production, are reduced in the dorsomedial prefrontal cortex (dmPFC) of stress-susceptible mice in chronic social defeat stress (CSDS) model. Conditional knockout of LDHA from the brain promotes depressive-like behaviors in both male and female mice, accompanied with reduced L-lactate levels and decreased neuronal excitability in the dmPFC. Moreover, these phenotypes could be duplicated by knockdown of LDHA in the dmPFC or specifically in astrocytes. In contrast, overexpression of LDHA reverses these phenotypic changes in CSDS-susceptible mice. Mechanistic studies demonstrate that L-lactate promotes neuronal excitability through monocarboxylic acid transporter 2 (MCT2) and by inhibiting large-conductance Ca

Indexed as

AstrocytesLactic AcidAnimalsCarrier ProteinsFemaleLactate Dehydrogenase 5L-Lactate DehydrogenaseMaleMiceProteomicsCarrier ProteinsLactate Dehydrogenase 5Lactic AcidL-Lactate Dehydrogenase

Identifiers

PMID36759610
PMCPMC9911790
OpenAlexW4319812687

What OpenQuestion holds

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LicenceCC BY
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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.