Evidence map›Paper›PMID 33235205›Full record

ArticleNature communications2020

Endocannabinoid signaling regulates the reinforcing and psychostimulant effects of ketamine in mice.

Wei Xu, Hongchun Li, Liang Wang, Jiamei Zhang, Chunqi Liu, Xuemei Wan, Xiaochong Liu, Yiming Hu, Qiyao Fang, Yuanyuan Xiao and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  4. Multi-level therapeutic actions of cannabidiol in ketamine-induced schizophrenia psychopathology in male rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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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

15 authors at 2 institutions in 1 country.

Wei XuNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Hongchun LiNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Liang WangNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Jiamei ZhangNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Chunqi LiuNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Xuemei WanNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Xiaochong LiuNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Yiming HuNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Qiyao FangNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Yuanyuan XiaoNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Qian BuNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Hongbo WangMinistry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, 264005, Yantai, People's Republic of China.
Jingwei TianMinistry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, 264005, Yantai, People's Republic of China.
Yinglan ZhaoNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China.
Xiaobo CenNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, People's Republic of China. xbcen@scu.edu.cn.ORCID 0000-0002-9760-5238
Sichuan University · CNYantai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The abuse potential of ketamine limits its clinical application, but the precise mechanism remains largely unclear. Here we discovered that ketamine significantly remodels the endocannabinoid-related lipidome and activates 2-arachidonoylglycerol (2-AG) signaling in the dorsal striatum (caudate nucleus and putamen, CPu) of mice. Elevated 2-AG in the CPu is essential for the psychostimulant and reinforcing effects of ketamine, whereas blockade of the cannabinoid CB1 receptor, a predominant 2-AG receptor, attenuates ketamine-induced remodeling of neuronal dendrite structure and neurobehaviors. Ketamine represses the transcription of the monoacylglycerol lipase (MAGL) gene by promoting the expression of PRDM5, a negative transcription factor of the MAGL gene, leading to increased 2-AG production. Genetic overexpression of MAGL or silencing of PRDM5 expression in the CPu robustly reduces 2-AG production and ketamine effects. Collectively, endocannabinoid signaling plays a critical role in mediating the psychostimulant and reinforcing properties of ketamine.

Indexed as

DNA-Binding ProteinsMonoacylglycerol LipasesTranscription FactorsAnimalsArachidonic AcidsCannabinoid Receptor AgonistsCaudate NucleusEndocannabinoidsGene ExpressionGene Expression RegulationGlyceridesKetamineMiceNeuronsReceptor, Cannabinoid, CB1Signal TransductionArachidonic AcidsCannabinoid Receptor AgonistsDNA-Binding ProteinsEndocannabinoidsGlyceridesglyceryl 2-arachidonateKetamineMonoacylglycerol LipasesPRDM5 protein, mouseReceptor, Cannabinoid, CB1Transcription Factors

Identifiers

PMID33235205
PMCPMC7686380
OpenAlexW3107486322

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.