Modulation of Presynaptic GABA Release by Oxidative Stress in Mechanically-isolated Rat Cerebral Cortical Neurons

Reactive oxygen species (ROS), which include hydrogen peroxide (H(2)O(2)), the superoxide anion (O(2) (-).), and the hydroxyl radical (OH.), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated...

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Published inThe Korean journal of physiology & pharmacology Vol. 14; no. 3; pp. 127 - 132
Main Authors Hahm, Eu-Teum, Seo, Jung-Woo, Hur, Jinyoung, Cho, Young-Wuk
Format Journal Article
LanguageEnglish
Published Korea (South) The Korean Physiological Society and The Korean Society of Pharmacology 01.06.2010
대한약리학회
Subjects
Original
약리학
Oxidative stress
Gamma-aminobutyric acid
Hydrogen peroxide
Inhibitory postsynaptic potentials
Online AccessGet full text
ISSN1226-4512
2093-3827
DOI10.4196/kjpp.2010.14.3.127

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Abstract Reactive oxygen species (ROS), which include hydrogen peroxide (H(2)O(2)), the superoxide anion (O(2) (-).), and the hydroxyl radical (OH.), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of H(2)O(2) on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at -60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM H(2)O(2) gradually potentiated mIPSCs. This potentiating effect of H(2)O(2) was blocked by the pretreatment with either 10,000-unit/mL catalase or 300-microM N-acetyl-cysteine. The potentiating effect of H(2)O(2) was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N-(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity.
AbstractList Reactive oxygen species (ROS), which include hydrogen peroxide (H2O2), the superoxide anion (O2−․), and the hydroxyl radical (OH․), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of H2O2 on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at −60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM H2O2 gradually potentiated mIPSCs. This potentiating effect of H2O2 was blocked by the pretreatment with either 10,000-unit/mL catalase or 300-μM N-acetyl-cysteine. The potentiating effect of H2O2 was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N-(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity. KCI Citation Count: 3
Reactive oxygen species (ROS), which include hydrogen peroxide (H(2)O(2)), the superoxide anion (O(2) (-).), and the hydroxyl radical (OH.), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of H(2)O(2) on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at -60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM H(2)O(2) gradually potentiated mIPSCs. This potentiating effect of H(2)O(2) was blocked by the pretreatment with either 10,000-unit/mL catalase or 300-microM N-acetyl-cysteine. The potentiating effect of H(2)O(2) was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N-(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity.
Reactive oxygen species (ROS), which include hydrogen peroxide (H 2 O 2 ), the superoxide anion (O 2 - ·), and the hydroxyl radical (OH·), are generated as by-products of oxidative metabolism in cells. The cerebral cortex has been found to be particularly vulnerable to production of ROS associated with conditions such as ischemia-reperfusion, Parkinson's disease, and aging. To investigate the effect of ROS on inhibitory GABAergic synaptic transmission, we examined the electrophysiological mechanisms of the modulatory effect of H 2 O 2 on GABAergic miniature inhibitory postsynaptic current (mIPSCs) in mechanically isolated rat cerebral cortical neurons retaining intact synaptic boutons. The membrane potential was voltage-clamped at -60 mV and mIPSCs were recorded and analyzed. Superfusion of 1-mM H 2 O 2 gradually potentiated mIPSCs. This potentiating effect of H 2 O 2 was blocked by the pretreatment with either 10,000-unit/mL catalase or 300-µM N-acetyl-cysteine. The potentiating effect of H 2 O 2 was occluded by an adenylate cyclase activator, forskolin, and was blocked by a protein kinase A inhibitor, N -(2-[p-bromocinnamylamino] ethyl)-5-isoquinolinesulfonamide hydrochloride. This study indicates that oxidative stress may potentiate presynaptic GABA release through the mechanism of cAMP-dependent protein kinase A (PKA)-dependent pathways, which may result in the inhibition of the cerebral cortex neuronal activity.
Author Seo, Jung-Woo
Hahm, Eu-Teum
Cho, Young-Wuk
Hur, Jinyoung
AuthorAffiliation Department of Physiology, Biomedical Science Institute and Medical Research Center for Reactive Oxygen Species, Kyung Hee University School of Medicine, Seoul 130-701, Korea
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DocumentTitleAlternate Modulation of Presynaptic GABA Release by Oxidative Stress in Mechanically-isolated Rat Cerebral Cortical Neurons
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Keywords Oxidative stress
Gamma-aminobutyric acid
Hydrogen peroxide
Inhibitory postsynaptic potentials
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Notes Eu-Teum Hahm and Jung-Woo Seo contributed equally to the present work.
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Snippet Reactive oxygen species (ROS), which include hydrogen peroxide (H(2)O(2)), the superoxide anion (O(2) (-).), and the hydroxyl radical (OH.), are generated as...
Reactive oxygen species (ROS), which include hydrogen peroxide (H 2 O 2 ), the superoxide anion (O 2 - ·), and the hydroxyl radical (OH·), are generated as...
Reactive oxygen species (ROS), which include hydrogen peroxide (H2O2), the superoxide anion (O2−․), and the hydroxyl radical (OH․), are generated as...
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Title Modulation of Presynaptic GABA Release by Oxidative Stress in Mechanically-isolated Rat Cerebral Cortical Neurons
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