Evidence map›Paper›PMID 39915158›Full record

ArticleBritish journal of anaesthesia2025

Striatal neurones expressing D1 dopamine receptors modulate consciousness in sevoflurane but not propofol anaesthesia in mice.

Kang Zhou, Zi-Jun Hou, Xu-Liang Jiang, Yu-Jie Xiao, Lin-Chen Zhang, Wei Xu, Bo Xiong, Wei-Min Qu, Yu-Guang Huang, Zhi-Li Huang and 1 more

Abstract read
In one paragraph

Article in British journal of anaesthesia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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

11 authors.

Kang ZhouDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Joint International Research Laboratory of Sleep, Fudan University, Shanghai, China; Department of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Zi-Jun HouDepartment of Anesthesiology, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Xu-Liang JiangDepartment of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Yu-Jie XiaoDepartment of Anesthesiology, Central South University, Changsha, Hunan, China.
Lin-Chen ZhangDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Joint International Research Laboratory of Sleep, Fudan University, Shanghai, China.
Wei XuDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Joint International Research Laboratory of Sleep, Fudan University, Shanghai, China.
Bo XiongDepartment of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Wei-Min QuDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Joint International Research Laboratory of Sleep, Fudan University, Shanghai, China.
Yu-Guang HuangDepartment of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. Electronic address: garypumch@163.com.
Zhi-Li HuangDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Joint International Research Laboratory of Sleep, Fudan University, Shanghai, China; Department of Anesthesiology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Electronic address: huangzl@fudan.edu.cn.
Lu WangDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Joint International Research Laboratory of Sleep, Fudan University, Shanghai, China. Electronic address: luwang1@fudan.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSevoflurane and propofol are the most widely used inhaled and i.v. general anaesthetics, respectively. The mechanisms by which sevoflurane and propofol induce loss of consciousness (LOC) remain unclear. Recent studies implicate the brain dopaminergic circuit in anaesthetic-induced LOC and the cortical-striatal-thalamic-cortical loop in decoding consciousness. We investigated the contribution of the dorsal striatum, which is a critical interface between the dopaminergic circuit and the cortical-striatal-thalamic-cortical loop, in sevoflurane and propofol anaesthesia.

methodsElectroencephalography and electromyography recordings and righting reflex tests were used to determine LOC and recovery of consciousness (ROC). The activity of D1 dopamine receptor (D1R)-expressing neurones in the dorsal striatum was monitored using fibre photometry, and regulated using optogenetic and chemogenetic methods in D1R-Cre mice.

resultsPopulation activities of striatal D1R neurones began to decrease before LOC and gradually returned after ROC. During sevoflurane anaesthesia, optogenetic activation of striatal D1R neurones induced ROC at cortical and behavioural levels in steady-state anaesthesia and promoted cortical activation in deep burst suppression anaesthesia. Chemogenetic inhibition of striatal D1R neurones accelerated induction (from 242.0 [46.1] to 194.0 [26.9] s; P=0.010) and delayed emergence (from 93.5 [21.2] to 133.5 [33.9] s; P=0.005), whereas chemogenetic activation of these neurones accelerated emergence (from 107 [23.7] to 81.3 [16.1] s; P=0.011). However, neither optogenetic nor chemogenetic manipulation of striatal D1R neurones had any effects on propofol anaesthesia.

conclusionsStriatal D1R neurones modulate the state of consciousness in sevoflurane anaesthesia, but not in propofol anaesthesia.

Indexed as

Anesthetics, InhalationAnesthetics, IntravenousConsciousnessCorpus StriatumNeuronsPropofolReceptors, Dopamine D1SevofluraneAnimalsElectroencephalographyMaleMiceMice, Inbred C57BLMice, TransgenicAnesthetics, InhalationAnesthetics, IntravenousPropofolReceptors, Dopamine D1Sevofluranechemogeneticsconsciousnessdorsal striatumoptogeneticspropofolsevoflurane

Identifiers

PMID39915158
PMCPMC11947605

What OpenQuestion holds

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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.