Evidence map›Paper›PMID 19442588›Full record

ArticleAutonomic neuroscience : basic & clinical2009

Reactive oxygen species modulate neuronal excitability in rat intrinsic cardiac ganglia.

K A Whyte, R C Hogg, J Dyavanapalli, A A Harper, D J Adams

Open access · hybridAbstract read
In one paragraph

Article in Autonomic neuroscience : basic & clinical, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  4. Redox Regulation of KAntioxidants & redox signaling · 2024
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  17. Reactive oxygen species alters the electrophysiological properties and raises [Ca2+]i in intracardiac ganglion neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2010
    Article
  18. Article
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 2 countries.

K A WhyteSchool of Biomedical Sciences, University of Queensland, Brisbane QLD 4072, Australia.
R C Hogg
J Dyavanapalli
A A Harper
D J Adams
University of Queensland · AUUniversity of Dundee · GB

Funding

British Heart Foundation PG/06/132/21753
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are produced as by-products of oxidative metabolism and occur in the heart during ischemia and coronary artery reperfusion. The effects of ROS on the electrophysiological properties of intracardiac neurons were investigated in the intracardiac ganglion (ICG) plexus in situ and in dissociated neurons from neonatal and adult rat hearts using the whole-cell patch clamp recording configuration. Bath application of ROS donors, hydrogen peroxide (H(2)O(2)) and tert-butyl hydroperoxide (t-BHP) hyperpolarized, and increased the action potential duration of both neonatal and adult ICG neurons. This action was also recorded in ICG neurons in an adult in situ ganglion preparation. H(2)O(2) and t-BHP also inhibited voltage-gated calcium channel (VGCC) currents and shifted the current-voltage (I-V) relationship to more hyperpolarized potentials. In contrast, H(2)O(2) increased the amplitude of the delayed rectifier K(+) current in neonatal ICG neurons. In neonatal ICG neurons, bath application of either superoxide dismutase (SOD) or catalase, scavengers of ROS, prior to H(2)O(2) attenuated the hyperpolarizing shift but not the inhibition of VGCC by H(2)O(2). In contrast, in adult ICG neurons, application of SOD alone had no effect upon either VGCC current amplitude or the I-V relationship, whereas application of SOD prior to H(2)O(2) exposure abolished both the H(2)O(2)-mediated hyperpolarizing shift and inhibition. These data indicate that ROS alter depolarization-activated Ca(2+) and K(+) conductances which underlie neuronal excitability of ICG neurons. This affects action potential duration and therefore probably modifies autonomic control of the heart during ischemia/reperfusion.

Indexed as

Action PotentialsAge FactorsAnimalsAnimals, NewbornBarium CompoundsBiophysical PhenomenaCalcium Channel BlockersChloridesDose-Response Relationship, DrugElectric StimulationFemaleGanglia, AutonomicHydrogen PeroxideIon Channel GatingMyocardiumNeuronsbarium chlorideBarium CompoundsCalcium Channel BlockersChloridesHydrogen PeroxideOxidantsPotassium Channel BlockersReactive Oxygen Speciestert-ButylhydroperoxideTetraethylammonium

Identifiers

PMID19442588
PMCPMC2751833
OpenAlexW2066785856

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.