File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Nitric oxide inhibits delayed rectifier potassium currents in cultured hippocampal neurons via S-nitrosylation

TitleNitric oxide inhibits delayed rectifier potassium currents in cultured hippocampal neurons via S-nitrosylation
Authors
KeywordsHippocampal neuron
NO
Patch clamp
Potassium channels
S-nitrosylation
Issue Date2006
Citation
Progress In Biochemistry And Biophysics, 2006, v. 33 n. 3, p. 241-246 How to Cite?
AbstractThe modulating action and mechanism of endogenous nitric oxide (NO) on the delayed rectifier potassium currents in cultured hippocampal neurons were examined using whole-cell patch clamp techniques. L-arginine (L-Arg, 2 mmol/L), a substrate of NO synthases, significantly suppressed the delayed rectifier K+ currents in hippocampal neurons, while its isomer D-arginine (D-Arg, 2 mmol/L) exerted no effect. Moreover, pretreatment with NO synthase inhibitor L-NAME (0.5 mmol/L) completely blocked the suppressing effect by L-Arg, indicating that L-Arg exerted its modulation by producing NO but not by itself. No effect was found on the L-Arg-induced inhibition by 10 min pretreatment of 10 μmol/L ODQ (a specific inhibitor of guanylate cyclase). In contrast, thiol-alkylating agent N-ethylmaleimide (1 mmol/L) completely precluded L-Arg-induced inhibition on the whole K+ currents. The results indicate that endogenous NO modulates the delayed rectifier K + currents in cultured hippocampal neurons mostly through S-nitrosylation.
Persistent Identifierhttp://hdl.handle.net/10722/81368
ISSN
2015 Impact Factor: 0.224
2015 SCImago Journal Rankings: 0.138
References

 

DC FieldValueLanguage
dc.contributor.authorWang, CFen_HK
dc.contributor.authorChen, Men_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorGao, TMen_HK
dc.date.accessioned2010-09-06T08:16:50Z-
dc.date.available2010-09-06T08:16:50Z-
dc.date.issued2006en_HK
dc.identifier.citationProgress In Biochemistry And Biophysics, 2006, v. 33 n. 3, p. 241-246en_HK
dc.identifier.issn1000-3282en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81368-
dc.description.abstractThe modulating action and mechanism of endogenous nitric oxide (NO) on the delayed rectifier potassium currents in cultured hippocampal neurons were examined using whole-cell patch clamp techniques. L-arginine (L-Arg, 2 mmol/L), a substrate of NO synthases, significantly suppressed the delayed rectifier K+ currents in hippocampal neurons, while its isomer D-arginine (D-Arg, 2 mmol/L) exerted no effect. Moreover, pretreatment with NO synthase inhibitor L-NAME (0.5 mmol/L) completely blocked the suppressing effect by L-Arg, indicating that L-Arg exerted its modulation by producing NO but not by itself. No effect was found on the L-Arg-induced inhibition by 10 min pretreatment of 10 μmol/L ODQ (a specific inhibitor of guanylate cyclase). In contrast, thiol-alkylating agent N-ethylmaleimide (1 mmol/L) completely precluded L-Arg-induced inhibition on the whole K+ currents. The results indicate that endogenous NO modulates the delayed rectifier K + currents in cultured hippocampal neurons mostly through S-nitrosylation.en_HK
dc.languageengen_HK
dc.relation.ispartofProgress in Biochemistry and Biophysicsen_HK
dc.subjectHippocampal neuronen_HK
dc.subjectNOen_HK
dc.subjectPatch clampen_HK
dc.subjectPotassium channelsen_HK
dc.subjectS-nitrosylationen_HK
dc.titleNitric oxide inhibits delayed rectifier potassium currents in cultured hippocampal neurons via S-nitrosylationen_HK
dc.typeArticleen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.scopuseid_2-s2.0-33744950102en_HK
dc.identifier.hkuros122292en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33744950102&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume33en_HK
dc.identifier.issue3en_HK
dc.identifier.spage241en_HK
dc.identifier.epage246en_HK
dc.publisher.placeChinaen_HK
dc.identifier.scopusauthoridWang, CF=14009100600en_HK
dc.identifier.scopusauthoridChen, M=35285618500en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridGao, TM=7101845480en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats