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Article: Role of voltage-gated Na+ channels in hypoxia-induced neuronal injuries

TitleRole of voltage-gated Na+ channels in hypoxia-induced neuronal injuries
Authors
KeywordsCA1
Hippocampus
Hypoxia
Tetrodotoxin
Voltage-gated Na+ channel
Issue Date2000
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP
Citation
Clinical And Experimental Pharmacology And Physiology, 2000, v. 27 n. 8, p. 569-574 How to Cite?
Abstract1. Mammalian neurons in the central nervous system are vulnerable to oxygen deprivation. In clinical conditions, such as stroke or apnoea, permanent loss of neuronal functions can occur within minutes of severe hypoxia. 2. Recent studies have focused on the role of Na+ in acute neuronal responses to hypoxia. These studies have shown that the influx of extracellular Na+ is an important factor in hypoxia-induced injury and that blockade of voltage-gated Na+ channels reduces hypoxic responses and injury of neurons. Yet, the mechanism underlying the effect of blockade of Na+ channels on hypoxic injury is unclear. 3. The aim of the present review is to discuss the above topics given the current understanding of the role of Na+ channels in hypoxia and its implications on therapeutic strategy for preventing hypoxia-induced neurological damage. 4. It has been known that the maintenance of ionic homeostasis and membrane properties in neurons are improved by reducing the activity of voltaged-gated Na+ channels during acute hypoxia. 5. Recent studies suggest that persistent Na+ current and Na+-dependent exchangers may play a role in Na+ influx and neuronal injury during hypoxia. 6. The neuroprotective action of blockers of the Na+ channel may also he via the improved maintenance of intracellular energy levels because the action is dependent on cellular energy levels and extracellular glucose during hypoxia. 7. Hence, the blockade of voltage-gated Na+ channels reduces the excitability of neurons, Na+ influx and the accumulation of intracellular Na+. These improve the ionic homeostasis and cellular energy levels and, thus, prevent hypoxia-induced neuronal injury and neuronal damage mediated by Ca2+ overload.
Persistent Identifierhttp://hdl.handle.net/10722/81354
ISSN
2012 Impact Factor: 2.16
2015 SCImago Journal Rankings: 0.944
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T08:16:41Z-
dc.date.available2010-09-06T08:16:41Z-
dc.date.issued2000en_HK
dc.identifier.citationClinical And Experimental Pharmacology And Physiology, 2000, v. 27 n. 8, p. 569-574en_HK
dc.identifier.issn0305-1870en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81354-
dc.description.abstract1. Mammalian neurons in the central nervous system are vulnerable to oxygen deprivation. In clinical conditions, such as stroke or apnoea, permanent loss of neuronal functions can occur within minutes of severe hypoxia. 2. Recent studies have focused on the role of Na+ in acute neuronal responses to hypoxia. These studies have shown that the influx of extracellular Na+ is an important factor in hypoxia-induced injury and that blockade of voltage-gated Na+ channels reduces hypoxic responses and injury of neurons. Yet, the mechanism underlying the effect of blockade of Na+ channels on hypoxic injury is unclear. 3. The aim of the present review is to discuss the above topics given the current understanding of the role of Na+ channels in hypoxia and its implications on therapeutic strategy for preventing hypoxia-induced neurological damage. 4. It has been known that the maintenance of ionic homeostasis and membrane properties in neurons are improved by reducing the activity of voltaged-gated Na+ channels during acute hypoxia. 5. Recent studies suggest that persistent Na+ current and Na+-dependent exchangers may play a role in Na+ influx and neuronal injury during hypoxia. 6. The neuroprotective action of blockers of the Na+ channel may also he via the improved maintenance of intracellular energy levels because the action is dependent on cellular energy levels and extracellular glucose during hypoxia. 7. Hence, the blockade of voltage-gated Na+ channels reduces the excitability of neurons, Na+ influx and the accumulation of intracellular Na+. These improve the ionic homeostasis and cellular energy levels and, thus, prevent hypoxia-induced neuronal injury and neuronal damage mediated by Ca2+ overload.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEPen_HK
dc.relation.ispartofClinical and Experimental Pharmacology and Physiologyen_HK
dc.subjectCA1en_HK
dc.subjectHippocampusen_HK
dc.subjectHypoxiaen_HK
dc.subjectTetrodotoxinen_HK
dc.subjectVoltage-gated Na+ channelen_HK
dc.titleRole of voltage-gated Na+ channels in hypoxia-induced neuronal injuriesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0305-1870&volume=27 &issue=8&spage=569&epage=574&date=2000&atitle=Role+of+voltage-gated+Na++channels+in+hypoxia-induced+neuronal+injuriesen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1440-1681.2000.03309.xen_HK
dc.identifier.pmid10901384-
dc.identifier.scopuseid_2-s2.0-0033918667en_HK
dc.identifier.hkuros53333en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033918667&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue8en_HK
dc.identifier.spage569en_HK
dc.identifier.epage574en_HK
dc.identifier.isiWOS:000087562100001-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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