Evidence map›Paper›PMID 27650924›Full record

ArticleScientific reports2016

Neuronal networks provide rapid neuroprotection against spreading toxicity.

Andrew J Samson, Graham Robertson, Michele Zagnoni, Christopher N Connolly

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

25 citing papers in PubMed, 219 citations in OpenAlex.

  1. Review
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  7. Review
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  9. Review
  10. Lab-on-Chip Microsystems forFrontiers in bioengineering and biotechnology · 2022
    Review
  11. Article
  12. Article
  13. Human mini-brain models.Nature biomedical engineering · 2021
    Review
  14. Article
  15. Article
  16. Super-Resolution Infrared Imaging of Polymorphic Amyloid Aggregates Directly in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020
    Article
  17. Review
  18. Article
  19. Review
  20. Stem cells technology: a powerful tool behind new brain treatments.Drug delivery and translational research · 2018
    Review
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 1 institution in 1 country.

Andrew J SamsonDivision of Neuroscience, School of Medicine, University of Dundee, Dundee, DD1 9SY, Scotland, Uk.
Graham RobertsonCentre for Microsystems and Photonics, Department of Electronic and Electrical Engineering, University of Strathclyde, Glasgow, G1 1XW, Scotland, Uk.
Michele ZagnoniCentre for Microsystems and Photonics, Department of Electronic and Electrical Engineering, University of Strathclyde, Glasgow, G1 1XW, Scotland, Uk.
Christopher N ConnollyDivision of Neuroscience, School of Medicine, University of Dundee, Dundee, DD1 9SY, Scotland, Uk.
University of Dundee · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

Acute secondary neuronal cell death, as seen in neurodegenerative disease, cerebral ischemia (stroke) and traumatic brain injury (TBI), drives spreading neurotoxicity into surrounding, undamaged, brain areas. This spreading toxicity occurs via two mechanisms, synaptic toxicity through hyperactivity, and excitotoxicity following the accumulation of extracellular glutamate. To date, there are no fast-acting therapeutic tools capable of terminating secondary spreading toxicity within a time frame relevant to the emergency treatment of stroke or TBI patients. Here, using hippocampal neurons (DIV 15-20) cultured in microfluidic devices in order to deliver a localized excitotoxic insult, we replicate secondary spreading toxicity and demonstrate that this process is driven by GluN2B receptors. In addition to the modeling of spreading toxicity, this approach has uncovered a previously unknown, fast acting, GluN2A-dependent neuroprotective signaling mechanism. This mechanism utilizes the innate capacity of surrounding neuronal networks to provide protection against both forms of spreading neuronal toxicity, synaptic hyperactivity and direct glutamate excitotoxicity. Importantly, network neuroprotection against spreading toxicity can be effectively stimulated after an excitotoxic insult has been delivered, and may identify a new therapeutic window to limit brain damage.

Indexed as

NeuroprotectionAnimalsHippocampusNerve NetNeurotoxicity SyndromesRatsRats, Sprague-DawleyStroke

Identifiers

PMID27650924
PMCPMC5030638
OpenAlexW2522811111

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.