title: An ATP-dependent inwardly rectifying potassium channel, KAB-2 (Kir4. 1), in cochlear stria vascularis of inner ear: its specific subcellular localization and correlation with the formation of endocochlear potential.
abstract: Cochlear endolymph has a highly positive potential of approximately +80 mV. This so-called endocochlear potential (EP) is essential for hearing. Although pivotal roles of K+ channels in the formation of EP have been suggested, the types and distribution of K+ channels in cochlea have not been characterized. Because EP was depressed by vascular perfusion of Ba2+, an inhibitor of inwardly rectifying K+ (Kir) channels, but not by either 4-aminopyridine or tetraethylammonium, we examined the expression of Kir channel subunits in cochlear stria vascularis, the tissue that is supposed to play the central role in the generation of positive EP. Of 11 members of the Kir channel family examined with reverse transcription-PCR, we could detect only expression of KAB-2 (Kir4.1) mRNA in stria vascularis. KAB-2 immunoreactivity was specifically localized at the basolateral membrane of marginal cells but not in either basal or intermediate cells. Developmental expression of KAB-2 in marginal cells paralleled formation of EP. Furthermore, deaf mutant mice (viable dominant spotting; WV/WV) expressed no KAB-2 in their marginal cells. These results suggest that KAB-2 in marginal cells may be critically involved in the generation of positive EP.
authors.affiliation: Department of Pharmacology II, Faculty of Medicine, Osaka University, Osaka 565, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Hibino
authors.forename: Y
authors.initials: Y
authors.lastname: Horio
authors.forename: A
authors.initials: A
authors.lastname: Inanobe
authors.forename: K
authors.initials: K
authors.lastname: Doi
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Gotow
authors.forename: Y
authors.initials: Y
authors.lastname: Uchiyama
authors.forename: M
authors.initials: M
authors.lastname: Kawamura
authors.forename: T
authors.initials: T
authors.lastname: Kubo
authors.forename: Y
authors.initials: Y
authors.lastname: Kurachi
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000375:Aging / Q000502:physiology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D003053:Cochlear Duct / Q000254:growth & development / Q000502:physiology*; D017931:DNA Primers; D003638:Deafness / Q000235:genetics; D004710:Endolymph / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D006168:Guinea Pigs; D007150:Immunohistochemistry; D051379:Mice; D008818:Mice, Neurologic Mutants; D016133:Polymerase Chain Reaction; D015221:Potassium Channels / Q000096:biosynthesis / Q000187:drug effects / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; D013347:Subcellular Fractions / Q000502:physiology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014158:Transcription, Genetic
chemical_list: D017931:DNA Primers; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; D013757:Tetraethylammonium Compounds; D001464:Barium; D019789:Tetraethylammonium; D015761:4-Aminopyridine