Evidence map›Paper›PMID 22832569›Full record

ArticleJournal of neurophysiology2012

Mitochondrial dysfunction induced by heat stress in cultured rat CNS neurons.

Michael G White, Osama Saleh, Doris Nonner, Ellen F Barrett, Carlos T Moraes, John N Barrett

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2012. 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
1.2field-weighted citation impact, top 23% 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, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Macronutrient modulation of mRNA and microRNA function in animals: A review.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2020
    Review
  19. Article
  20. Brain diseases in changing climate.Environmental research · 2019
    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

6 authors at 1 institution in 1 country.

Michael G WhiteDept. of Physiology and Biophysics, Univ. of Miami Miller School of Medicine, Miami, FL 33101, USA.
Osama Saleh
Doris Nonner
Ellen F Barrett
Carlos T Moraes
John N Barrett
University of Miami · US

Funding

SETTING THE STAGE FOR REPLACEMENT OF MITOCHONDRIAL GENESR01EY010804 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 1995 to 2025
$9.4M
Mitochondrial Dysfunction in Neurodegeneration and Compensatory ApproachesR01AG036871 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2010 to 2020
$3.3M
Synapses,Channels, and Transduction in NeuroscienceT32NS007044 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MULLER, KENNETH J · 1985 to 2010
$2.2M
MYELINATED AXONS AND MOTOR TERMINALS--FUNCTIONAL STUDIESR01NS012404 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BARRETT, ELLEN F · 1985 to 2006
$1.7M
NEUROTROPHIN PROTECTION OF STRESSED CHOLINERGIC NEURONSR01NS012207 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BARRETT, JOHN N · 1985 to 2003
$1.3M
NEI NIH HHS R01 EY 010804NEI NIH HHS R01 EY010804NIA NIH HHS R01 AG036871NINDS NIH HHS 2T32 NS 07044NINDS NIH HHS R01 NS012207NINDS NIH HHS R01 NS012404NINDS NIH HHS R01 NS 12207NINDS NIH HHS R01 NS 12404NINDS NIH HHS T32 NS007044
6 · The paper itself

Abstract

Previous work demonstrated that hyperthermia (43°C for 2 h) results in delayed, apoptotic-like death in striatal neuronal cultures. We investigated early changes in mitochondrial function induced by this heat stress. Partial depolarization of the mitochondrial membrane potential (ΔΨ(m)) began about 1 h after the onset of hyperthermia and increased as the stress continued. When the heat stress ended, there was a partial recovery of ΔΨ(m), followed hours later by a progressive, irreversible depolarization of ΔΨ(m). During the heat stress, O(2) consumption initially increased but after 20-30 min began a progressive, irreversible decline to about one-half the initial rate by the end of the stress. The percentage of oligomycin-insensitive respiration increased during the heat stress, suggesting an increased mitochondrial leak conductance. Analysis using inhibitors and substrates for specific respiratory chain complexes indicated hyperthermia-induced dysfunction at or upstream of complex I. ATP levels remained near normal for ∼4 h after the heat stress. Mitochondrial movement along neurites was markedly slowed during and just after the heat stress. The early, persisting mitochondrial dysfunction described here likely contributes to the later (>10 h) caspase activation and neuronal death produced by this heat stress. Consistent with this idea, proton carrier-induced ΔΨ(m) depolarizations comparable in duration to those produced by the heat stress also reduced neuronal viability. Post-stress ΔΨ(m) depolarization and/or delayed neuronal death were modestly reduced/postponed by nicotinamide adenine dinucleotide, a calpain inhibitor, and increased expression of Bcl-xL.

Indexed as

Heat-Shock ResponseAdenosine TriphosphateAnimalsApoptosisBrainCalciumMembrane Potential, MitochondrialMitochondriaMitochondrial ProteinsNeuronsOligomycinsOxygenProtonsRatsRespirationAdenosine TriphosphateCalciumMitochondrial ProteinsOligomycinsOxygenProtons

Identifiers

PMID22832569
PMCPMC3545021
OpenAlexW1970134082

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.