Evidence map›Paper›PMID 28620235›Full record

ArticleScientific reports2017

A non-ionotropic activity of NMDA receptors contributes to glycine-induced neuroprotection in cerebral ischemia-reperfusion injury.

Juan Chen, Rong Hu, Huabao Liao, Ya Zhang, Ruixue Lei, Zhifeng Zhang, Yang Zhuang, Yu Wan, Ping Jin, Hua Feng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 55 citations in OpenAlex.

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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 at 4 institutions in 1 country.

Juan ChenDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China. chenjuan0828@163.com.
Rong HuDepartment of Neurosurgery, Southwest Hospital, Chongqing, 400038, China.
Huabao LiaoDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China.
Ya ZhangDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China.
Ruixue LeiDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China.
Zhifeng ZhangDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China.
Yang ZhuangDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China.
Yu WanDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China.
Ping JinDepartment of Neurology, the Central Hospital of Wuhan, Tongji Medical College of Huazhong University of Science & Technology, 26 Shengli Street, Wuhan, 430014, China.
Hua FengDepartment of Neurosurgery, Southwest Hospital, Chongqing, 400038, China.
Qi WanDepartment of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, Hubei, 430071, China. qwanwh@hotmail.com.
Wuhan University · CNSouthwest Hospital · CNHuazhong University of Science and Technology · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NMDA receptor (NMDAR) is known for its ionotropic function. But recent evidence suggests that NMDAR also has a non-ionotropic property. To determine the role of non-ionotropic activity of NMDARs in clinical relevant conditions, we tested the effect of glycine, a co-agonist of NMDARs, in rat middle cerebral artery occlusion (MCAO), an animal model of cerebral ischemia-reperfusion injury after the animals were injected with the NMDAR channel blocker MK-801 and the glycine receptor antagonist strychnine. We show that glycine reduces the infarct volume in the brain of ischemic stroke animals pre-injected with MK-801 and strychnine. The effect of glycine is sensitive to the antagonist of glycine-GluN1 binding site and blocked by Akt inhibition. In the neurobehavioral tests, glycine improves the functional recovery of stroke animals pre-injected with MK-801 and strychnine. This study suggests that glycine-induced neuroprotection is mediated in part by the non-ionotropic activity of NMDARs via Akt activation in cerebral ischemia-reperfusion injury.

Indexed as

NeuroprotectionAnimalsBrain IschemiaDisease Models, AnimalGlutamic AcidGlycineMaleProtein BindingProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRatsReceptors, N-Methyl-D-AspartateReperfusion InjurySeverity of Illness IndexGlutamic AcidGlycineProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, N-Methyl-D-Aspartate

Identifiers

PMID28620235
PMCPMC5472592
OpenAlexW2621781675

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.