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THIK-1 (K(2P)13.1) is a small-conductance background K+ channel in rat trigeminal ganglion neurons

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dc.contributor.authorKang, Dawon-
dc.contributor.authorHogan, James O.-
dc.contributor.authorKim, Donghee-
dc.date.accessioned2022-12-26T23:04:32Z-
dc.date.available2022-12-26T23:04:32Z-
dc.date.issued2014-07-
dc.identifier.issn0031-6768-
dc.identifier.issn1432-2013-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/18913-
dc.description.abstractThe goal of this study was to determine the molecular identity of a small-conductance (similar to 5-pS) background K+ channel expressed in trigeminal ganglion (TG) neurons. We tested the hypothesis that the 5-pS channel is a K-2P channel by comparing the pharmacological and single-channel properties of THIK-1 expressed in HEK293 cells. As reported earlier, whole-cell THIK-1 current was inhibited by halothane and activated by arachidonic acid. Among 25 additional modulators tested, bupivacaine (100 mu M), quinidine (50 mu M) and Ba2+ (3 mM) and cold (10 A degrees C) were most effective inhibitors of THIK-1 current (> 50 % inhibition). In cell-attached patches with high KCl in the pipette and bath solutions, THIK-1 produced a small-conductance (similar to 5 pS) channel with a weak inwardly rectifying current-voltage relationship. Halothane, bupivacaine and cold inhibited the single-channel activities of both THIK-1 and the 5-pS channel in TG neurons, whereas arachidonic acid augmented them. THIK-1 expressed in HEK293 cells and the 5-pS channels in TG neurons were insensitive to hypoxia. Reverse transcriptase-PCR, Western blot and immunocytochemical analyses suggested that THIK-1 mRNA and protein were expressed in TG neurons. These results show that THIK-1 is functionally expressed in TG neurons and contributes to the background K+ conductance.-
dc.format.extent12-
dc.language영어-
dc.language.isoENG-
dc.publisherSPRINGER-
dc.titleTHIK-1 (K(2P)13.1) is a small-conductance background K+ channel in rat trigeminal ganglion neurons-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1007/s00424-013-1358-1-
dc.identifier.scopusid2-s2.0-84904625983-
dc.identifier.wosid000338224700005-
dc.identifier.bibliographicCitationPFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, v.466, no.7, pp 1289 - 1300-
dc.citation.titlePFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY-
dc.citation.volume466-
dc.citation.number7-
dc.citation.startPage1289-
dc.citation.endPage1300-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaPhysiology-
dc.relation.journalWebOfScienceCategoryPhysiology-
dc.subject.keywordPlusPOTASSIUM CHANNELS-
dc.subject.keywordPlusCAROTID-BODY-
dc.subject.keywordPlusK-2P CHANNELS-
dc.subject.keywordPlusKIDNEY-CELLS-
dc.subject.keywordPlusHALOTHANE-
dc.subject.keywordPlusTRPM8-
dc.subject.keywordPlusCOLD-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusTASK2-
dc.subject.keywordPlusTASK-1/TASK-3-
dc.subject.keywordAuthorArachidonic acid-
dc.subject.keywordAuthorBackground K+ channel-
dc.subject.keywordAuthorCold-
dc.subject.keywordAuthorHalothane-
dc.subject.keywordAuthorHypoxia-
dc.subject.keywordAuthorTwo-pore domain-
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