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Article: Sodium homeostasis in rat hippocampal slices during oxygen and glucose deprivation: Role of voltage-sensitive sodium channels

TitleSodium homeostasis in rat hippocampal slices during oxygen and glucose deprivation: Role of voltage-sensitive sodium channels
Authors
Issue Date1999
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 1999, v. 275 n. 1, p. 41-44 How to Cite?
AbstractThe breakdown in brain ionic homeostasis during energy deprivation (anoxic depolarization [AD]) is intimately linked to neuronal injury. We studied the role of one particular route of Na + influx, voltage-sensitive Na + channels, in the AD induced by O 2 and/or glucose deprivation. We recorded extracellular Na + concentration ([Na +](e)) and direct current potential (DCP) in the CA1 stratum pyramidale of hippocampal slices using Na +-selective microelectrodes. Tetrodotoxin (0.1-1 μM) delayed the occurrence of AD and reduced the peak change in both [Na +](e) and DCP during AD. However the tetrodotoxin effects were overcome by a concomitant reduction in extracellular glucose during anoxia. We conclude that: (1) the activation of voltage-gated Na + channels is involved in the triggering of AD; (2) there may be a critical level of energy depletion when AD occurs and different mechanisms may underlie AD during hypoxia, compared to O 2 and glucose deprivation. Copyright (C) 1999 Elsevier Science Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/171664
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_US
dc.contributor.authorCroning, MDRen_US
dc.contributor.authorHaddad, GGen_US
dc.date.accessioned2012-10-30T06:16:14Z-
dc.date.available2012-10-30T06:16:14Z-
dc.date.issued1999en_US
dc.identifier.citationNeuroscience Letters, 1999, v. 275 n. 1, p. 41-44en_US
dc.identifier.issn0304-3940en_US
dc.identifier.urihttp://hdl.handle.net/10722/171664-
dc.description.abstractThe breakdown in brain ionic homeostasis during energy deprivation (anoxic depolarization [AD]) is intimately linked to neuronal injury. We studied the role of one particular route of Na + influx, voltage-sensitive Na + channels, in the AD induced by O 2 and/or glucose deprivation. We recorded extracellular Na + concentration ([Na +](e)) and direct current potential (DCP) in the CA1 stratum pyramidale of hippocampal slices using Na +-selective microelectrodes. Tetrodotoxin (0.1-1 μM) delayed the occurrence of AD and reduced the peak change in both [Na +](e) and DCP during AD. However the tetrodotoxin effects were overcome by a concomitant reduction in extracellular glucose during anoxia. We conclude that: (1) the activation of voltage-gated Na + channels is involved in the triggering of AD; (2) there may be a critical level of energy depletion when AD occurs and different mechanisms may underlie AD during hypoxia, compared to O 2 and glucose deprivation. Copyright (C) 1999 Elsevier Science Ireland Ltd.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_US
dc.relation.ispartofNeuroscience Lettersen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Hypoxiaen_US
dc.subject.meshEvoked Potentialsen_US
dc.subject.meshGlucose - Deficiencyen_US
dc.subject.meshHippocampus - Metabolism - Physiologyen_US
dc.subject.meshHomeostasisen_US
dc.subject.meshIon Channel Gatingen_US
dc.subject.meshMicroelectrodesen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSodium - Metabolismen_US
dc.subject.meshSodium Channels - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshTetrodotoxin - Pharmacologyen_US
dc.titleSodium homeostasis in rat hippocampal slices during oxygen and glucose deprivation: Role of voltage-sensitive sodium channelsen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0304-3940(99)00728-4en_US
dc.identifier.pmid10554980-
dc.identifier.scopuseid_2-s2.0-0032828805en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032828805&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume275en_US
dc.identifier.issue1en_US
dc.identifier.spage41en_US
dc.identifier.epage44en_US
dc.identifier.isiWOS:000083392000011-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US
dc.identifier.scopusauthoridCroning, MDR=6603151438en_US
dc.identifier.scopusauthoridHaddad, GG=7201349499en_US

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