Evidence map›Paper›PMID 31847911›Full record

ArticleJournal of neuroinflammation2019

Stress-induced microglial activation occurs through β-adrenergic receptor: noradrenaline as a key neurotransmitter in microglial activation.

Shuei Sugama, Takato Takenouchi, Makoto Hashimoto, Hisayuki Ohata, Yasuhiro Takenaka, Yoshihiko Kakinuma

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 107 citations in OpenAlex.

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1 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Shuei SugamaDepartment of Physiology, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo, 113-8602, Japan. sugama@nms.ac.jp.ORCID http://orcid.org/0000-0002-3065-6452
Takato TakenouchiInstitute of Agrobiological Sciences, National Agriculture and Food Research Organization, 1-2 Ohwashi, Tsukuba, Ibaraki, 305-8634, Japan.
Makoto HashimotoDivision of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-0057, Japan.
Hisayuki OhataDepartment of Physiology, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo, 113-8602, Japan.
Yasuhiro TakenakaDepartment of Physiology, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo, 113-8602, Japan.
Yoshihiko KakinumaDepartment of Physiology, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo, 113-8602, Japan.
Nippon Medical School · JPNational Agriculture and Food Research Organization · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe involvement of microglia in neuroinflammatory responses has been extensively demonstrated. Recent animal studies have shown that exposure to either acute or chronic stress induces robust microglial activation in the brain. In the present study, we investigated the underlying mechanism of brain microglial activation by acute stress.

methodsWe first looked at the spatial distribution of the noradrenaline (NA)-synthesizing enzyme, DBH (dopamine β-hydroxylase), in comparison with NA receptors-β1, β2, and β3 adrenergic receptors (β1-AR, β2-AR, and β3-AR)-after which we examined the effects of the β-blocker propranolol and α-blockers prazosin and yohimbine on stress-induced microglial activation. Finally, we compared stress-induced microglial activation between wild-type (WT) mice and double-knockout (DKO) mice lacking β1-AR and β2-AR.

resultsThe results demonstrated that (1) microglial activation occurred in most studied brain regions, including the hippocampus (HC), thalamus (TM), and hypothalamus (HT); (2) within these three brain regions, the NA-synthesizing enzyme DBH was densely stained in the neuronal fibers; (3) β1-AR and β2-AR, but not β3-AR, are detected in the whole brain, and β1-AR and β2-AR are co-localized with microglial cells, as observed by laser scanning microscopy; (4) β-blocker treatment inhibited microglial activation in terms of morphology and count through the whole brain; α-blockers did not show such effect; (5) unlike WT mice, DKO mice exhibited substantial inhibition of stress-induced microglial activation in the brain.

conclusionsWe demonstrate that neurons/microglia may interact with NA via β1-AR and β2-AR.

Indexed as

AnimalsBrainMaleMiceMice, KnockoutMicrogliaNeuronsNorepinephrinePsychological DistressRats, Inbred F344Receptors, Adrenergic, betaRestraint, PhysicalStress, PhysiologicalNorepinephrineReceptors, Adrenergic, betaBrainCNSMicrogliaNeuroimmunomodulationRestraint stress

Identifiers

PMID31847911
PMCPMC6916186
OpenAlexW2996373213

What OpenQuestion holds

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LicenceCC BY
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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.