Evidence map›Paper›PMID 12562896›Full record

ArticleThe Journal of physiology2003

Hydrogen-peroxide-induced toxicity of rat striatal neurones involves activation of a non-selective cation channel.

M A Smith, P S Herson, K Lee, R D Pinnock, M L J Ashford

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 75 citations in OpenAlex.

  1. A conserved mechanism couples cytosolic domain movements to pore gating in the TRPM2 channel.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Review
  3. Article
  4. Hydrogen Peroxide Gates a Voltage-Dependent Cation Current inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  5. Article
  6. Drosophila TRPA1 isoforms detect UV light via photochemical production of H2O2.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  7. Hydrogen peroxide increases GABAA receptor-mediated tonic current in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  8. Review
  9. Androgen and PARP-1 regulation of TRPM2 channels after ischemic injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Article
  10. Review
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  12. Article
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  17. Sex differences in neuroprotection provided by inhibition of TRPM2 channels following experimental stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011
    Article
  18. H2O2: a dynamic neuromodulator.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2011
    Review
  19. Article
  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 2 institutions in 1 country.

M A SmithDepartment of Biomedical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK.
P S Herson
K Lee
R D Pinnock
M L J Ashford
University of Aberdeen · GBPfizer (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Striatal neurones are particularly vulnerable to hypoxia/ischaemia-induced damage, and free radicals are thought to be prime mediators of this neuronal destruction. It has been shown that hydrogen peroxide (H2O2), through the production of free radicals, induces rat insulinoma cell death by activation of a non-selective cation channel, which leads to irreversible cell depolarization and unregulated Ca2+ entry into the cell. In the study presented here, we demonstrate that a subpopulation of striatal neurones (medium spiny neurones) is depolarized by H2O2 through the production of free radicals. Cell-attached recordings from rat cultured striatal neurones demonstrate that exposure to H2O2 opens a large-conductance channel that is characterized by extremely long open times (seconds). Inside-out recordings show that cytoplasmically applied beta-nicotinamide adenine dinucleotide activates a channel with little voltage dependence, a linear current-voltage relationship and a single-channel conductance of between 70 and 90 pS. This channel is permeable to Na+, K+ and Ca2+ ions. Fura-2 imaging from cultured striatal neurones reveals that H2O2 exposure induces a biphasic intracellular Ca2+ increase in a subpopulation of neurones, the second, later phase resulting in Ca2+ overload. This later component of the Ca2+ response is dependent on the presence of extracellular Ca2+ and is independent of synaptic activity or voltage-gated Ca2+ channel opening. Consequently, this channel may be an important contributor to free radical-induced selective striatal neurone destruction. These results are remarkably similar to those observed for insulinoma cells and suggest that this family of non-selective cation channels has a widespread distribution in mammalian tissues.

Indexed as

AnimalsCalciumCationsCells, CulturedCorpus StriatumElectrophysiologyHydrogen PeroxideIntracellular MembranesIon ChannelsNeuronsOxidantsRatsRats, Sprague-DawleyCalciumCationsHydrogen PeroxideIon ChannelsOxidants

Identifiers

PMID12562896
PMCPMC2342643
OpenAlexW2136440137

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.