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Article: Anoxia-induced depolarization in CA1 hippocampal neurons: Role of Na+- dependent mechanisms

TitleAnoxia-induced depolarization in CA1 hippocampal neurons: Role of Na+- dependent mechanisms
Authors
KeywordsAmiloride
Anoxia
CA1
Hippocampus
Sodium
Tetrodotoxin
Issue Date1997
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
Citation
Brain Research, 1997, v. 762 n. 1-2, p. 97-102 How to Cite?
AbstractWe have previously shown that (1) removal of extracellular sodium (Na+) reduces the anoxia-induced depolarization in neurons in brain-slice preparations and (2) amiloride, which blocks Na+-dependent exchangers, prevents anoxic injury in cultured neocortical neurons. Since anoxia-induced depolarization has been linked to neuronal injury, we have examined in this study the role of Na+-dependent exchangers and voltage-gated Na+ channels in the maintenance of membrane properties of CA1 neurons at rest and during acute hypoxia. We recorded intracellularly from CA1 neurons in hippocampal slices, monitored V(m) and measured input resistance (R(m)) with periodic injections of negative current. We found that tetrodotoxin (TTX, 1 μM) hyperpolarized CA1 neurons at rest and significantly attenuated both the rate of depolarization (ΔV(m)/dt) and the rate of decline of R(m) (ΔR(m)/dt) by about 60% during the early phase of hypoxia. The effect of TTX was dose- dependent. Amiloride (1 mM) decreased V(m) and increased R(m) in the resting condition but changed little the effect of hypoxia on neuronal function. Benzamil and 5-(N-ethyl-N-isopropyl)-2',4'-amiloride (EIPA), two specific inhibitors of Na+ dependent exchangers, were similar to amiloride in their effect. We conclude that neuronal membrane properties are better maintained during anoxia by reducing the activity of TTX-sensitive channels and not by the action of Na+-dependent exchangers.
Persistent Identifierhttp://hdl.handle.net/10722/81155
ISSN
2015 Impact Factor: 2.561
2015 SCImago Journal Rankings: 1.351
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_HK
dc.contributor.authorHaddad, GGen_HK
dc.date.accessioned2010-09-06T08:14:27Z-
dc.date.available2010-09-06T08:14:27Z-
dc.date.issued1997en_HK
dc.identifier.citationBrain Research, 1997, v. 762 n. 1-2, p. 97-102en_HK
dc.identifier.issn0006-8993en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81155-
dc.description.abstractWe have previously shown that (1) removal of extracellular sodium (Na+) reduces the anoxia-induced depolarization in neurons in brain-slice preparations and (2) amiloride, which blocks Na+-dependent exchangers, prevents anoxic injury in cultured neocortical neurons. Since anoxia-induced depolarization has been linked to neuronal injury, we have examined in this study the role of Na+-dependent exchangers and voltage-gated Na+ channels in the maintenance of membrane properties of CA1 neurons at rest and during acute hypoxia. We recorded intracellularly from CA1 neurons in hippocampal slices, monitored V(m) and measured input resistance (R(m)) with periodic injections of negative current. We found that tetrodotoxin (TTX, 1 μM) hyperpolarized CA1 neurons at rest and significantly attenuated both the rate of depolarization (ΔV(m)/dt) and the rate of decline of R(m) (ΔR(m)/dt) by about 60% during the early phase of hypoxia. The effect of TTX was dose- dependent. Amiloride (1 mM) decreased V(m) and increased R(m) in the resting condition but changed little the effect of hypoxia on neuronal function. Benzamil and 5-(N-ethyl-N-isopropyl)-2',4'-amiloride (EIPA), two specific inhibitors of Na+ dependent exchangers, were similar to amiloride in their effect. We conclude that neuronal membrane properties are better maintained during anoxia by reducing the activity of TTX-sensitive channels and not by the action of Na+-dependent exchangers.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_HK
dc.relation.ispartofBrain Researchen_HK
dc.rightsBrain Research. Copyright © Elsevier BV.en_HK
dc.subjectAmilorideen_HK
dc.subjectAnoxiaen_HK
dc.subjectCA1en_HK
dc.subjectHippocampusen_HK
dc.subjectSodiumen_HK
dc.subjectTetrodotoxinen_HK
dc.titleAnoxia-induced depolarization in CA1 hippocampal neurons: Role of Na+- dependent mechanismsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-8993&volume=762&spage=97&epage=102&date=1997&atitle=Anoxia-induced+depolarization+in+CA1++hippocampal+neurons:+Role+of+Na+-dependent+mechanismsen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0006-8993(97)00371-5en_HK
dc.identifier.pmid9262163-
dc.identifier.scopuseid_2-s2.0-0030740747en_HK
dc.identifier.hkuros36782en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030740747&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume762en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage97en_HK
dc.identifier.epage102en_HK
dc.identifier.isiWOS:A1997XL77500012-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridHaddad, GG=7201349499en_HK

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