Evidence map›Paper›PMID 28398653›Full record

ArticleJournal of neurochemistry2017

The noble gas xenon provides protection and trophic stimulation to midbrain dopamine neurons.

Jérémie Lavaur, Déborah Le Nogue, Marc Lemaire, Jan Pype, Géraldine Farjot, Etienne C Hirsch, Patrick P Michel

Open access · hybridAbstract read
In one paragraph

Article in Journal of neurochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 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

7 authors at 2 institutions in 1 country.

Jérémie LavaurSorbonne Universités, UPMC Univ Paris 06, Inserm, CNRS, Institut du Cerveau et de la Moelle épinière (ICM), Hôpital Pitié-Salpêtrière, Paris, France.
Déborah Le NogueSorbonne Universités, UPMC Univ Paris 06, Inserm, CNRS, Institut du Cerveau et de la Moelle épinière (ICM), Hôpital Pitié-Salpêtrière, Paris, France.
Marc LemaireAir Liquide Santé International, Medical R&D Paris, Saclay Research Center, Jouy-en Josas, France.
Jan PypeAir Liquide Santé International, Medical R&D Paris, Saclay Research Center, Jouy-en Josas, France.
Géraldine FarjotAir Liquide Santé International, Medical R&D Paris, Saclay Research Center, Jouy-en Josas, France.
Etienne C HirschSorbonne Universités, UPMC Univ Paris 06, Inserm, CNRS, Institut du Cerveau et de la Moelle épinière (ICM), Hôpital Pitié-Salpêtrière, Paris, France.
Patrick P MichelSorbonne Universités, UPMC Univ Paris 06, Inserm, CNRS, Institut du Cerveau et de la Moelle épinière (ICM), Hôpital Pitié-Salpêtrière, Paris, France.ORCID 0000-0001-5607-3119
Centre National de la Recherche Scientifique · FRAir Liquide (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite its low chemical reactivity, the noble gas xenon possesses a remarkable spectrum of biological effects. In particular, xenon is a strong neuroprotectant in preclinical models of hypoxic-ischemic brain injury. In this study, we wished to determine whether xenon retained its neuroprotective potential in experimental settings that model the progressive loss of midbrain dopamine (DA) neurons in Parkinson's disease. Using rat midbrain cultures, we established that xenon was partially protective for DA neurons through either direct or indirect effects on these neurons. So, when DA neurons were exposed to l-trans-pyrrolidine-2,4-dicarboxylic acid so as to increase ambient glutamate levels and generate slow and sustained excitotoxicity, the effect of xenon on DA neurons was direct. The vitamin E analog Trolox also partially rescued DA neurons in this setting and enhanced neuroprotection by xenon. However, in the situation where DA cell death was spontaneous, the protection of DA neurons by xenon appeared indirect as it occurred through the repression of a mechanism mediated by proliferating glial cells, presumably astrocytes and their precursor cells. Xenon also exerted trophic effects for DA neurons in this paradigm. The effects of xenon were mimicked and improved by the N-methyl-d-aspartate glutamate receptor antagonist memantine and xenon itself appeared to work by antagonizing N-methyl-d-aspartate receptors. Note that another noble gas argon could not reproduce xenon effects. Overall, present data indicate that xenon can provide protection and trophic support to DA neurons that are vulnerable in Parkinson's disease. This suggests that xenon might have some therapeutic value for this disorder.

Indexed as

Anesthetics, InhalationAnimalsAntioxidantsCell DeathCells, CulturedChromansDicarboxylic AcidsDopaminergic NeuronsExcitatory Amino Acid AntagonistsMemantineMesencephalonNeuroprotective AgentsOrgan Culture TechniquesPyrrolidinesRatsRats, Wistar6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acidAnesthetics, InhalationAntioxidantsChromansDicarboxylic AcidsExcitatory Amino Acid AntagonistsMemantineNeuroprotective Agentspyrrolidine-2,4-dicarboxylic acidPyrrolidinesXenonastroglial cellsdopamine neuronsglutamateneurodegenerationNMDAxenon

Identifiers

PMID28398653
PMCPMC5518208
OpenAlexW2607410782

What OpenQuestion 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 OpenQuestion graph.