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dc.contributor.authorHsu, Hung-Te
dc.contributor.authorTseng, Yu-Ting
dc.contributor.authorLo, Yi-Ching
dc.contributor.authorWu, Sheng-Nan
dc.date.accessioned2021-01-15T05:21:49Z
dc.date.available2021-01-15T05:21:49Z
dc.date.issued2014
dc.identifier.issn1471-2202en_US
dc.identifier.doi10.1186/s12868-014-0135-1en_US
dc.identifier.urihttp://hdl.handle.net/10072/401161
dc.description.abstractBackground: Naringenin (NGEN) is a citrus bioflavonoid known to have beneficial health properties; however, the ionic mechanism of its actions remains largely unclear. In this study, we attempted to evaluate the possible effects of NGEN on K+ currents in NSC-34 neuronal cells and in HEK293T cells expressing α-hSlo. Results: NGEN increased M-type K+ current (IK(M)) in a concentration-dependent manner with an EC50 value of 9.8 μM in NSC-34 cells. NGEN shifted the activation curve of IK(M) conductance to the more negative potentials. In cell-attached recordings, NGEN or flupirtine enhanced the activity of M-type K+ (KM) channels with no changes in single-channel amplitude. NGEN (10 μM) had minimal effect on erg-mediated K+ currents. Under cell-attached voltage-clamp recordings, NGEN decreased the frequency of spontaneous action currents and further application of linopirdine can reverse NGEN-induced inhibition of firing. In HEK293T cells expressing α-hSlo, this compound increased the amplitude of Ca2+-activated K+ current (IK(Ca)). Under inside-out recordings, NGEN applied to the intracellular side of the detached patch enhanced the activity of large-conductance Ca2+-activated K+ (BKCa) channels. Moreover, from the study of a modeled neuron, burst firing of simulated action potentials (APs) was reduced in the presence of the increased conductances of both KM and KCa channels. Fast-slow analysis of AP bursting from this model also revealed that as the conductances of both KM and BKCa channels were increased by two-fold, the voltage nullcline was shifted in an upward direction accompanied by the compression of burst trajectory. Conclusions: The present results demonstrate that activation of both KM and BKCa channels caused by NGEN might combine to influence neuronal activity if similar channels were functionally co-expressed in central neurons in vivo.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglish
dc.language.isoeng
dc.publisherSpringer Science and Business Media LLCen_US
dc.relation.ispartofpagefrom135en_US
dc.relation.ispartofissue1en_US
dc.relation.ispartofjournalBMC Neuroscienceen_US
dc.relation.ispartofvolume15en_US
dc.subject.fieldofresearchBiochemistry and Cell Biologyen_US
dc.subject.fieldofresearchNeurosciencesen_US
dc.subject.fieldofresearchCognitive Sciencesen_US
dc.subject.fieldofresearchcode0601en_US
dc.subject.fieldofresearchcode1109en_US
dc.subject.fieldofresearchcode1702en_US
dc.titleAbility of naringenin, a bioflavonoid, to activate M-type potassium current in motor neuron-like cells and to increase BKCa-channel activity in HEK293T cells transfected with α-hSlo subuniten_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Articlesen_US
dcterms.bibliographicCitationHsu, H-T; Tseng, Y-T; Lo, Y-C; Wu, S-N, Ability of naringenin, a bioflavonoid, to activate M-type potassium current in motor neuron-like cells and to increase BKCa-channel activity in HEK293T cells transfected with α-hSlo subunit, BMC Neuroscience, 2014, 15 (1), pp. 135en_US
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/en_US
dc.date.updated2021-01-15T05:18:49Z
dc.description.versionVersion of Record (VoR)en_US
gro.rights.copyright© 2015 Hsu et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.en_US
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gro.griffith.authorTseng, Tammy


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