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Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons

Nitric oxide (NO) is an important signaling molecule involved in nociceptive transmission. It can induce analgesic and hyperalgesic effects in the central nervous system. In this study, patch-clamp recording was used to investigate the effect of NO on neuronal excitability in substantia gelatinosa (...

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Autores principales: Park, A-Reum, Lee, Hae In, Semjid, Dejidnorov, Kim, Do Kyung, Chun, Sang Woo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3910459/
https://www.ncbi.nlm.nih.gov/pubmed/24511395
http://dx.doi.org/10.1155/2014/628531
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author Park, A-Reum
Lee, Hae In
Semjid, Dejidnorov
Kim, Do Kyung
Chun, Sang Woo
author_facet Park, A-Reum
Lee, Hae In
Semjid, Dejidnorov
Kim, Do Kyung
Chun, Sang Woo
author_sort Park, A-Reum
collection PubMed
description Nitric oxide (NO) is an important signaling molecule involved in nociceptive transmission. It can induce analgesic and hyperalgesic effects in the central nervous system. In this study, patch-clamp recording was used to investigate the effect of NO on neuronal excitability in substantia gelatinosa (SG) neurons of the spinal cord. Different concentrations of sodium nitroprusside (SNP; NO donor) induced a dual effect on the excitability of neuronal membrane: 1 mM of SNP evoked membrane hyperpolarization and an outward current, whereas 10 µM induced depolarization of the membrane and an inward current. These effects were prevented by hemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO) (NO scavengers), phenyl N-tert-butylnitrone (PBN; nonspecific reactive oxygen species scavenger), and through inhibition of soluble guanylyl cyclase (sGC). Pretreatment with n-ethylmaleimide (NEM; thiol-alkylating agent) also decreased effects of both 1 mM and 10 µM SNP, suggesting that these responses were mediated by direct S-nitrosylation. Charybdotoxin (CTX) and tetraethylammonium (TEA) (large-conductance Ca(2+)-activated K(+) channel blockers) and glybenclamide (ATP-sensitive K(+) channel blocker) decreased SNP-induced hyperpolarization. La(3+) (nonspecific cation channel blocker), but not Cs(+) (hyperpolarization-activated K(+) channel blocker), blocked SNP-induced membrane depolarization. In conclusion, NO dually affects neuronal excitability in a concentration-dependent manner via modification of various K(+) channels.
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spelling pubmed-39104592014-02-09 Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons Park, A-Reum Lee, Hae In Semjid, Dejidnorov Kim, Do Kyung Chun, Sang Woo Neural Plast Research Article Nitric oxide (NO) is an important signaling molecule involved in nociceptive transmission. It can induce analgesic and hyperalgesic effects in the central nervous system. In this study, patch-clamp recording was used to investigate the effect of NO on neuronal excitability in substantia gelatinosa (SG) neurons of the spinal cord. Different concentrations of sodium nitroprusside (SNP; NO donor) induced a dual effect on the excitability of neuronal membrane: 1 mM of SNP evoked membrane hyperpolarization and an outward current, whereas 10 µM induced depolarization of the membrane and an inward current. These effects were prevented by hemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO) (NO scavengers), phenyl N-tert-butylnitrone (PBN; nonspecific reactive oxygen species scavenger), and through inhibition of soluble guanylyl cyclase (sGC). Pretreatment with n-ethylmaleimide (NEM; thiol-alkylating agent) also decreased effects of both 1 mM and 10 µM SNP, suggesting that these responses were mediated by direct S-nitrosylation. Charybdotoxin (CTX) and tetraethylammonium (TEA) (large-conductance Ca(2+)-activated K(+) channel blockers) and glybenclamide (ATP-sensitive K(+) channel blocker) decreased SNP-induced hyperpolarization. La(3+) (nonspecific cation channel blocker), but not Cs(+) (hyperpolarization-activated K(+) channel blocker), blocked SNP-induced membrane depolarization. In conclusion, NO dually affects neuronal excitability in a concentration-dependent manner via modification of various K(+) channels. Hindawi Publishing Corporation 2014 2014-01-08 /pmc/articles/PMC3910459/ /pubmed/24511395 http://dx.doi.org/10.1155/2014/628531 Text en Copyright © 2014 A-Reum Park et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Park, A-Reum
Lee, Hae In
Semjid, Dejidnorov
Kim, Do Kyung
Chun, Sang Woo
Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
title Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
title_full Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
title_fullStr Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
title_full_unstemmed Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
title_short Dual Effect of Exogenous Nitric Oxide on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
title_sort dual effect of exogenous nitric oxide on neuronal excitability in rat substantia gelatinosa neurons
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3910459/
https://www.ncbi.nlm.nih.gov/pubmed/24511395
http://dx.doi.org/10.1155/2014/628531
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