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Article: Elevated endogenous nitric oxide increases Ca 2+ flux via L-type Ca 2+ channels by S-nitrosylation in rat hippocampal neurons during severe hypoxia and in vitro ischemia

TitleElevated endogenous nitric oxide increases Ca 2+ flux via L-type Ca 2+ channels by S-nitrosylation in rat hippocampal neurons during severe hypoxia and in vitro ischemia
Authors
Issue Date2007
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
Citation
Free Radical Biology And Medicine, 2007, v. 42 n. 1, p. 52-63 How to Cite?
AbstractNitric oxide (NO) mediates pathogenic changes in the brain subsequent to energy deprivation; yet the NO mechanism involved in the early events remains unclear. We examined the acute effects of severe hypoxia and oxygen-glucose deprivation (OGD) on the endogenous NO production and the NO-mediated pathways involved in the intracellular calcium ([Ca 2+] i) response in the rat hippocampal neurons. The levels of NO and [Ca 2+] i in the CA1 region of the slices rapidly elevated in hypoxia and were more prominent in OGD, measured by the electrochemical method and spectrofluorometry, respectively. The NO and [Ca 2+] i responses were enhanced by L-arginine and were reduced by NO synthase inhibitors, suggesting that the endogenous NO increases the [Ca 2+] i response to energy deprivation. Nickel and nifedipine significantly decreased the NO and [Ca 2+] i responses to hypoxia and OGD, indicating an involvement of L-type Ca 2+ channels in the NO-mediated mechanisms. In addition, the [Ca 2+] i responses were attenuated by ODQ or KT5823, inhibitors of the cGMP-PKG pathway, and by acivicin, an inhibitor of γ-glutamyl transpeptidase for S-nitrosylation, and by the thiol-alkylating agent N-ethylmaleimide (NEM). Moreover, L-type Ca 2+ currents in cultured hippocampal neurons with whole-cell recording were significantly increased by L-arginine and were decreased by L-NAME. Pretreatment with NO synthase inhibitors or NEM but not ODQ abolished the effect of L-arginine on the Ca 2+ currents. Also, vitamin C, which decomposes nitrosothiol but not disulfide by reduction, reversed the change in the Ca 2+ current with L-arginine. Taken together, the results suggest that an elevated endogenous NO production enhances the influx of Ca 2+ via the hippocampal L-type Ca 2+ channel by S-nitrosylation during an initial phase of energy deprivation. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171751
ISSN
2015 Impact Factor: 5.784
2015 SCImago Journal Rankings: 2.468
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTjong, YWen_US
dc.contributor.authorJian, Ken_US
dc.contributor.authorLi, Men_US
dc.contributor.authorChen, Men_US
dc.contributor.authorGao, TMen_US
dc.contributor.authorFung, MLen_US
dc.date.accessioned2012-10-30T06:16:47Z-
dc.date.available2012-10-30T06:16:47Z-
dc.date.issued2007en_US
dc.identifier.citationFree Radical Biology And Medicine, 2007, v. 42 n. 1, p. 52-63en_US
dc.identifier.issn0891-5849en_US
dc.identifier.urihttp://hdl.handle.net/10722/171751-
dc.description.abstractNitric oxide (NO) mediates pathogenic changes in the brain subsequent to energy deprivation; yet the NO mechanism involved in the early events remains unclear. We examined the acute effects of severe hypoxia and oxygen-glucose deprivation (OGD) on the endogenous NO production and the NO-mediated pathways involved in the intracellular calcium ([Ca 2+] i) response in the rat hippocampal neurons. The levels of NO and [Ca 2+] i in the CA1 region of the slices rapidly elevated in hypoxia and were more prominent in OGD, measured by the electrochemical method and spectrofluorometry, respectively. The NO and [Ca 2+] i responses were enhanced by L-arginine and were reduced by NO synthase inhibitors, suggesting that the endogenous NO increases the [Ca 2+] i response to energy deprivation. Nickel and nifedipine significantly decreased the NO and [Ca 2+] i responses to hypoxia and OGD, indicating an involvement of L-type Ca 2+ channels in the NO-mediated mechanisms. In addition, the [Ca 2+] i responses were attenuated by ODQ or KT5823, inhibitors of the cGMP-PKG pathway, and by acivicin, an inhibitor of γ-glutamyl transpeptidase for S-nitrosylation, and by the thiol-alkylating agent N-ethylmaleimide (NEM). Moreover, L-type Ca 2+ currents in cultured hippocampal neurons with whole-cell recording were significantly increased by L-arginine and were decreased by L-NAME. Pretreatment with NO synthase inhibitors or NEM but not ODQ abolished the effect of L-arginine on the Ca 2+ currents. Also, vitamin C, which decomposes nitrosothiol but not disulfide by reduction, reversed the change in the Ca 2+ current with L-arginine. Taken together, the results suggest that an elevated endogenous NO production enhances the influx of Ca 2+ via the hippocampal L-type Ca 2+ channel by S-nitrosylation during an initial phase of energy deprivation. © 2006 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomeden_US
dc.relation.ispartofFree Radical Biology and Medicineen_US
dc.rightsFree Radical Biology & Medicine. Copyright © Elsevier Inc.-
dc.subject.meshAnimalsen_US
dc.subject.meshArginine - Pharmacologyen_US
dc.subject.meshBrain Ischemia - Metabolism - Pathologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channels, L-Type - Metabolismen_US
dc.subject.meshCell Hypoxiaen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshFura-2en_US
dc.subject.meshHippocampus - Cytology - Metabolismen_US
dc.subject.meshNg-Nitroarginine Methyl Ester - Pharmacologyen_US
dc.subject.meshNeurons - Cytology - Metabolismen_US
dc.subject.meshNitric Oxide - Pharmacologyen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshOxygen - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshS-Nitrosothiols - Metabolismen_US
dc.titleElevated endogenous nitric oxide increases Ca 2+ flux via L-type Ca 2+ channels by S-nitrosylation in rat hippocampal neurons during severe hypoxia and in vitro ischemiaen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.emailTjong, YW: jefftjong@yahoo.com.hk-
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.freeradbiomed.2006.09.020en_US
dc.identifier.pmid17157193-
dc.identifier.scopuseid_2-s2.0-33751580333en_US
dc.identifier.hkuros128583-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33751580333&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume42en_US
dc.identifier.issue1en_US
dc.identifier.spage52en_US
dc.identifier.epage63en_US
dc.identifier.isiWOS:000242975200005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTjong, YW=6507176524en_US
dc.identifier.scopusauthoridJian, K=36929518800en_US
dc.identifier.scopusauthoridLi, M=15132223400en_US
dc.identifier.scopusauthoridChen, M=35285618500en_US
dc.identifier.scopusauthoridGao, TM=7101845480en_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US

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