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Article: Decreased large conductance Ca2+-activated K+ channel activity in dissociated CA1 hippocampal neurons in rats exposed to perinatal and postnatal hypoxia

TitleDecreased large conductance Ca2+-activated K+ channel activity in dissociated CA1 hippocampal neurons in rats exposed to perinatal and postnatal hypoxia
Authors
KeywordsCA1
Chronic hypoxia
Hippocampus
Oxygen deprivation
Potassium channel
Issue Date2002
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2002, v. 332 n. 3, p. 163-166 How to Cite?
AbstractHypoxia is a major cause of neonatal encephalopathy and seizures, and an increased neuronal excitability may be an underlying mechanism. To determine the role of Ca2+-activated K+ channels in hyperexcitability, we measured large unitary conductance (>200 pS, BKCa) currents in symmetrical 140/140 mM K+ using inside-out configuration in CA1 pyramidal cells acutely dissociated from the hippocampus of rats exposed to normoxia or hypoxia (at 10% inspired O2) for 4 weeks after birth. About 53% of the patches contained BKCa channels in the normoxic group, but only 20% in the hypoxic one. There were no differences in channel conductance or reversal potential between the groups. Yet, the open probability of BKCa channels was much less in hypoxic neurons than that in the control, because of a decrease in channel open time and a prolongation of the closed time. These were partially recovered by an oxidizing but not by reducing agent, suggesting an involvement of redox mechanism. Results indicate that the Ca2+-activated K+ channel activities in hippocampal CA1 neurons are modulated by hypoxia during maturation. The reduction in BKCa activity may contribute to hypoxia-induced neuronal hyperexcitability. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/81107
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGao, TMen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T08:13:54Z-
dc.date.available2010-09-06T08:13:54Z-
dc.date.issued2002en_HK
dc.identifier.citationNeuroscience Letters, 2002, v. 332 n. 3, p. 163-166en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81107-
dc.description.abstractHypoxia is a major cause of neonatal encephalopathy and seizures, and an increased neuronal excitability may be an underlying mechanism. To determine the role of Ca2+-activated K+ channels in hyperexcitability, we measured large unitary conductance (>200 pS, BKCa) currents in symmetrical 140/140 mM K+ using inside-out configuration in CA1 pyramidal cells acutely dissociated from the hippocampus of rats exposed to normoxia or hypoxia (at 10% inspired O2) for 4 weeks after birth. About 53% of the patches contained BKCa channels in the normoxic group, but only 20% in the hypoxic one. There were no differences in channel conductance or reversal potential between the groups. Yet, the open probability of BKCa channels was much less in hypoxic neurons than that in the control, because of a decrease in channel open time and a prolongation of the closed time. These were partially recovered by an oxidizing but not by reducing agent, suggesting an involvement of redox mechanism. Results indicate that the Ca2+-activated K+ channel activities in hippocampal CA1 neurons are modulated by hypoxia during maturation. The reduction in BKCa activity may contribute to hypoxia-induced neuronal hyperexcitability. © 2002 Elsevier Science Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.rightsNeuroscience Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectCA1en_HK
dc.subjectChronic hypoxiaen_HK
dc.subjectHippocampusen_HK
dc.subjectOxygen deprivationen_HK
dc.subjectPotassium channelen_HK
dc.titleDecreased large conductance Ca2+-activated K+ channel activity in dissociated CA1 hippocampal neurons in rats exposed to perinatal and postnatal hypoxiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3940&volume=332&spage=163&epage=166&date=2002&atitle=Decreased+large+conductance+Ca2+-activated+K++channel+activity+in+dissociated+CA1+hippocampal+neurons+in+rats+exposed+to+perinatal+and+postnatal+hypoxia.en_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/S0304-3940(02)00946-1en_HK
dc.identifier.pmid12399006en_HK
dc.identifier.scopuseid_2-s2.0-0037044708en_HK
dc.identifier.hkuros81763en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037044708&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume332en_HK
dc.identifier.issue3en_HK
dc.identifier.spage163en_HK
dc.identifier.epage166en_HK
dc.identifier.isiWOS:000179013300004-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridGao, TM=7101845480en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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