Evidence map›Paper›PMID 25228100›Full record

ArticleNeuroendocrinology2014

Glucocorticoids increase excitotoxic injury and inflammation in the hippocampus of adult male rats.

Shawn F Sorrells, Carolina D Munhoz, Nathan C Manley, Sandra Yen, Robert M Sapolsky

Open access · bronzeAbstract read
In one paragraph

Article in Neuroendocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.6field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Meta-analysis of cortical thickness abnormalities in medication-free patients with major depressive disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Pooled it
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  11. Effects of Longitudinal Changes in Neuroticism and Stress on Cognitive Decline.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2023
    Observational
  12. Article
  13. Article
  14. Brain vitamin DFrontiers in cellular neuroscience · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

5 authors at 2 institutions in 2 countries.

Shawn F SorrellsDepartment of Biology, Stanford University, Stanford, Calif., USA.
Carolina D Munhoz
Nathan C Manley
Sandra Yen
Robert M Sapolsky
Stanford University · USUniversidade de São Paulo · BR

Funding

Pro-inflammatory glucocorticoid effects in the CNSR01NS059918 · NINDS · STANFORD UNIVERSITY · PI SAPOLSKY, ROBERT M. · 2009 to 2010
$789k
The role of glucocorticoid signaling in immune cells during excitotoxicity.F31NS063491 · NINDS · STANFORD UNIVERSITY · PI SORRELLS, SHAWN · 2009 to 2010
$62k
NINDS NIH HHS F31 NS063491NINDS NIH HHS R01 NS059918
6 · The paper itself

Abstract

BACKGROUND/

aimsStress exacerbates neuron loss in many CNS injuries via the actions of adrenal glucocorticoid (GC) hormones. For some injuries, this GC endangerment of neurons is accompanied by greater immune cell activation in the CNS, a surprising outcome given the potent immunosuppressive properties of GCs.

methodsTo determine whether the effects of GCs on inflammation contribute to neuron death or result from it, we tested whether nonsteroidal anti-inflammatory drugs could protect neurons from GCs during kainic acid excitotoxicity in adrenalectomized male rats. We next measured GC effects on (1) chemokine production (CCL2 and CINC-1), (2) signals that suppress immune activation (CX3CL1, CD22, CD200, and TGF-β), and (3) NF-κB activity.

resultsConcurrent treatment with minocycline, but not indomethacin, prevented GC endangerment. GCs did not substantially affect CCL2, CINC-1, or baseline NF-κB activity, but they did suppress CX3CL1, CX3CR1, and CD22 expression in the hippocampus - factors that normally restrain inflammatory responses.

conclusionsThese findings demonstrate that cellular inflammation is not necessarily suppressed by GCs in the injured hippocampus; instead, GCs may worsen hippocampal neuron death, at least in part by increasing the neurotoxicity of CNS inflammation.

Indexed as

AdrenalectomyAnimalsAnti-Inflammatory Agents, Non-SteroidalCell DeathChemokinesDose-Response Relationship, DrugExcitatory Amino Acid AgonistsGlucocorticoidsHippocampusIndomethacinKainic AcidMaleMinocyclineNeuroimmunomodulationNeuronsNeuroprotective AgentsAnti-Inflammatory Agents, Non-SteroidalChemokinesExcitatory Amino Acid AgonistsGlucocorticoidsIndomethacinKainic AcidMinocyclineNeuroprotective Agents

Identifiers

PMID25228100
PMCPMC4304880
OpenAlexW2083795881

What OpenQuestion holds

Textmetadata
LicenceTDM
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.