Evidence map›Paper›PMID 28019006›Full record

ReviewNeurochemical research2017

Glucose and Intermediary Metabolism and Astrocyte-Neuron Interactions Following Neonatal Hypoxia-Ischemia in Rat.

Eva Brekke, Hester Rijkje Berger, Marius Widerøe, Ursula Sonnewald, Tora Sund Morken

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.5field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. A new perspective on HIV: effects of HIV on brain-heart axis.Frontiers in cardiovascular medicine · 2023
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

5 authors at 4 institutions in 2 countries.

Eva BrekkeDepartment of Neuroscience, Norwegian University of Science and Technology (NTNU), 7489, Trondheim, Norway.
Hester Rijkje BergerDepartment of Laboratory Medicine, Children's and Women's Health, NTNU, 7489, Trondheim, Norway.
Marius WiderøeDepartment of Circulation and Medical Imaging, NTNU, 7489, Trondheim, Norway.
Ursula SonnewaldDepartment of Neuroscience, Norwegian University of Science and Technology (NTNU), 7489, Trondheim, Norway.
Tora Sund MorkenDepartment of Laboratory Medicine, Children's and Women's Health, NTNU, 7489, Trondheim, Norway. tora.sund.morken@stolav.no.
St Olav's University Hospital · NONordland Hospital · NONorwegian University of Science and Technology · NOUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal hypoxia-ischemia (HI) and the delayed injury cascade that follows involve excitotoxicity, oxidative stress and mitochondrial failure. The susceptibility to excitotoxicity of the neonatal brain may be related to the capacity of astrocytes for glutamate uptake. Furthermore, the neonatal brain is vulnerable to oxidative stress, and the pentose phosphate pathway (PPP) may be of particular importance for limiting this kind of injury. Also, in the neonatal brain, neurons depend upon de novo synthesis of neurotransmitters via pyruvate carboxylase in astrocytes to increase neurotransmitter pools during normal brain development. Several recent publications describing intermediary brain metabolism following neonatal HI have yielded interesting results: (1) Following HI there is a prolonged depression of mitochondrial metabolism in agreement with emerging evidence of mitochondria as vulnerable targets in the delayed injury cascade. (2) Astrocytes, like neurons, are metabolically impaired following HI, and the degree of astrocytic malfunction may be an indicator of the outcome following hypoxic and hypoxic-ischemic brain injury. (3) Glutamate transfer from neurons to astrocytes is not increased following neonatal HI, which may imply that astrocytes fail to upregulate glutamate uptake in response to the massive glutamate release during HI, thus contributing to excitotoxicity. (4) In the neonatal brain, the activity of the PPP is reduced following HI, which may add to the susceptibility of the neonatal brain to oxidative stress. The present review aims to discuss the metabolic temporal alterations observed in the neonatal brain following HI.

Indexed as

AnimalsAnimals, NewbornAstrocytesBrainGlucoseHumansHypoxia-Ischemia, BrainNeuronsRatsGlucose13C NMRAstrocyte–neuron interactionsGlucose metabolismGlutamate–glutamine cycleNeonatal hypoxia–ischemiaPentose-phosphate-pathwayPyruvate carboxylation

Identifiers

PMID28019006
OpenAlexW2565583403

What OpenQuestion holds

Textmetadata
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.