Evidence map›Paper›PMID 25641742›Full record

ArticleJournal of neuroscience research2015

Tumor necrosis factor-α potentiates long-term potentiation in the rat dentate gyrus after acute hypoxia.

Audrey M Wall, Gatambwa Mukandala, Nigel H Greig, John J O'Connor

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 22% 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, 37 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

4 authors at 2 institutions in 2 countries.

Audrey M WallUCD School of Biomolecular and Biomedical Sciences, UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin, Ireland.
Gatambwa Mukandala
Nigel H Greig
John J O'Connor
University College Dublin · IENational Institutes of Health · US

Funding

Pro-inflammatory cytokine lowering anti-inflammatory drugsZIAAG000994 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2016 to 2025
$16.8M
Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
Intramural NIH HHS ZIA AG000311
6 · The paper itself

Abstract

An inadequate supply of oxygen in the brain may lead to an inflammatory response through neuronal and glial cells that can result in neuronal damage. Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that is released during acute hypoxia and can have neurotoxic or neuroprotective effects in the brain. Both TNF-α and interleukin-1β (IL-1β) have been shown by a number of research groups to alter synaptic scaling and also to inhibit long-term potentiation (LTP) in the hippocampus when induced by specific high-frequency stimulation (HFS) protocols. This study examines the effects of TNF-α on synaptic transmission and plasticity in hippocampal slices after acute hypoxia using two HFS protocols. Field excitatory postsynaptic potentials were elicited in the medial perforant pathway of the dentate gyrus. Exogenous TNF-α (5 ng/ml) attenuated LTP induced by theta burst stimulation but had no effect on LTP induced by a more prolonged HFS. Pretreatment with lipopolysaccharide (100 ng/ml) or TNF-α but not IL-1β (4 ng/ml) prior to a 30-min hypoxic insult resulted in a significant enhancement of LTP post hypoxia when induced by the HFS. Anti-TNF, 3,6'-dithiothalidomide (a TNF-α synthesis inhibitor), and SB203580 (a p38 MAPK inhibitor) significantly reduced this effect. These results indicate an important modulatory role for elevated TNF-α levels on LTP in the hippocampus after an acute hypoxic event.

Indexed as

AnimalsAnimals, NewbornAnti-Inflammatory Agents, Non-SteroidalCells, CulturedDentate GyrusElectric StimulationExcitatory Postsynaptic PotentialsHypoxiaImidazolesInterleukin-1betaIn Vitro TechniquesLipopolysaccharidesL-Lactate DehydrogenaseLong-Term PotentiationMalePatch-Clamp Techniques2-amino-5-phosphopentanoic acidAnti-Inflammatory Agents, Non-SteroidalImidazolesInterleukin-1betaLipopolysaccharidesL-Lactate DehydrogenasePyridinesSB 203580Tumor Necrosis Factor-alphaValine1,6′-dithiorevlimid3,6′-dithiothalidomideCNTO1081dentate gyrushigh-frequency stimulationhypoxiainterleukin-1βlong-term potentiationprolyl hydroxylase inhibitiontheta burst stimulationtumor necrosis factor-α

Identifiers

PMID25641742
PMCPMC5187981
OpenAlexW1502219667

What OpenQuestion holds

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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.