Evidence map›Paper›PMID 32264970›Full record

ArticleJournal of neuroinflammation2020

Hippocampal microglial activation triggers a neurotoxic-specific astrocyte response and mediates etomidate-induced long-term synaptic inhibition.

Dongliang Li, Mingming Chen, Tao Meng, Jianchun Fei

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

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  16. Foxq1 activates CB2R with oleamide to alleviate POCD.Brain pathology (Zurich, Switzerland) · 2025
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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

4 authors at 2 institutions in 1 country.

Dongliang LiDepartment of Anesthesiology, Qilu Hospital of Shandong University, Ji'nan, 250012, China.
Mingming ChenJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, 210009, China.
Tao MengDepartment of Anesthesiology, Qilu Hospital of Shandong University, Ji'nan, 250012, China.
Jianchun FeiDepartment of Anesthesiology, Qilu Hospital of Shandong University, Ji'nan, 250012, China. qlfeijc@163.com.
Qilu Hospital of Shandong University · CNChina Pharmaceutical University · CN

Funding

Natural Science Foundation of Shandong Province ZR2019MH133
6 · The paper itself

Abstract

backgroundAccumulating evidence has highlighted the importance of microglial and astrocyte responses in the pathological development of postoperative cognitive dysfunction (POCD). However, the mechanisms involved are not well understood.

methodsA perioperative neurocognitive disorders (PND) mouse model was generated by administering etomidate, and cognitive function was assessed using the Morris water maze and novel object recognition tests. Excitatory and inhibitory postsynaptic currents were recorded to analyze neuronal activity. In addition, microglia and astrocytes were isolated by magnetic-activated cell sorting, and genes that were activated in these cells were identified using quantitative polymerase chain reaction.

resultsWe observed dramatic cognitive impairment at 1 and 3 weeks after etomidate was administered to 18 month-old mice. Microglia and astrocytes isolated from the hippocampus showed significant microglial activation during the early pathological stage (i.e., 1 week after etomidate injection) and an A1-specific astrocyte response during the late pathological stage (i.e., 3 weeks after etomidate injection). Furthermore, when microglia were eliminated before etomidate was injected, the A1-specific astrocyte activation response was significantly reduced, and cognitive function improved. However, when microglia were eliminated after etomidate application, astrocyte activation and cognitive function were not significantly altered. In addition, activating microglia immediately after a sedative dose of etomidate was injected markedly increased A1-specific astrocyte activation and cognitive dysfunction.

conclusionsA1-specific astrocyte activation is triggered by activated microglia during the initial pathological stage of PND and induces long-term synaptic inhibition and cognitive deficiencies. These results improve our understanding of how PND develops and may suggest therapeutic targets.

Indexed as

AnimalsAstrocytesEtomidateHippocampusHypnotics and SedativesLong-Term Synaptic DepressionMaleMiceMicrogliaNeurotoxicity SyndromesPostoperative Cognitive ComplicationsEtomidateHypnotics and SedativesEPSCGeneral anestheticsInflammationIPSCmagnetic-activated cell-sortingSynaptic plasticity

Identifiers

PMID32264970
PMCPMC7140340
OpenAlexW3014781994

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LicenceCC BY
Read underepoch 390

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.