Reactive oxygen species modulate neuronal excitability in rat intrinsic cardiac ganglia

Whyte, K. A., Hogg, R. C., Dyavanapalli, J., Harper, A. A. and Adams, D. J. (2009) Reactive oxygen species modulate neuronal excitability in rat intrinsic cardiac ganglia. Autonomic Neuroscience: Basic and Clinical, 150 1-2: 45-52. doi:10.1016/j.autneu.2009.04.005

Author Whyte, K. A.
Hogg, R. C.
Dyavanapalli, J.
Harper, A. A.
Adams, D. J.
Title Reactive oxygen species modulate neuronal excitability in rat intrinsic cardiac ganglia
Journal name Autonomic Neuroscience: Basic and Clinical   Check publisher's open access policy
ISSN 1566-0702
Publication date 2009-10
Sub-type Article (original research)
DOI 10.1016/j.autneu.2009.04.005
Volume 150
Issue 1-2
Start page 45
End page 52
Total pages 8
Place of publication Amsterdam, Netherlands
Publisher Elsevier
Collection year 2010
Language eng
Formatted 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 intracardiacneurons 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 (H2O2) and tert-butyl hydroperoxide (t-BHP) hyperpolarized, and increased the action potential duration of both neonatal and adult ICG neurons. This actionwas also recorded in ICG neurons in
an adult in situ ganglion preparation. H2O2 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, H2O2 increased the amplitude of the delayed rectifier K+current in neonatal ICGneurons. In neonatal ICG neurons, bath
application of either superoxide dismutase (SOD) or catalase, scavengers of ROS, prior to H2O2 attenuated the hyperpolarizing shift but not the inhibition of VGCC by H2O2. In contrast, in adult ICG neurons, application of SODalone had no effect upon either VGCC current amplitude or the I–V relationship,whereas application of SOD prior to H2O2 exposure abolished both the H2O2-mediated hyperpolarizing shift and inhibition. These data indicate that ROS alter depolarization-activated Ca2+ 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.
Keyword Hydrogen peroxide
Intracardiac neuron
Voltage-gated calcium channel
Delayed rectifier potassium channel
K+ Channels
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2010 Higher Education Research Data Collection
Queensland Brain Institute Publications
School of Biomedical Sciences Publications
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Citation counts: TR Web of Science Citation Count  Cited 11 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 12 times in Scopus Article | Citations
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Created: Thu, 12 Nov 2009, 12:05:04 EST by Mr Andrew Martlew on behalf of School of Biomedical Sciences