title: Inwardly rectifying potassium channel Kir4.1 is localized at the calyx endings of vestibular afferents.
abstract: Inwardly rectifying potassium (Kir) channel Kir4.1 (also called Kcnj10) is expressed in various cells such as satellite glial cells. It is suggested that these cells would absorb excess accumulated K(+) from intercellular space which is surrounded by these cell membranes expressing Kir4.1. In the vestibular system, loss of Kir4.1 results in selective degeneration of type I hair cells despite normal development of type II hair cells. The mechanisms underlying this developmental disorder have been unclear, because it was thought that Kir4.1 is only expressed in glial cells throughout the entire nervous system. Here, we show that Kir4.1 is expressed not only in glial cells but also in neurons of the mouse vestibular system. In the vestibular ganglion, Kir4.1 mRNA is transcribed in both satellite cells and neuronal somata, whereas Kir4.1 protein is expressed only in satellite cells. On the other hand, in the vestibular sensory epithelia, Kir4.1 protein is localized at the calyx endings of vestibular afferents, which surround type I hair cells. Kir4.1 protein expression in the vestibular sensory epithelia is detected beginning after birth, and its localization gradually adopts a calyceal shape until type I hair cells are mature. Kir4.1 localized at the calyx endings may play a role in the K(+)-buffering action of vestibular afferents surrounding type I hair cells.
authors.affiliation: Department of Otorhinolaryngology, The Jikei University School of Medicine, Tokyo 105-8461, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Udagawa
authors.forename: N
authors.initials: N
authors.lastname: Tatsumi
authors.forename: T
authors.initials: T
authors.lastname: Tachibana
authors.forename: Y
authors.initials: Y
authors.lastname: Negishi
authors.forename: H
authors.initials: H
authors.lastname: Saijo
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Yaguchi
authors.forename: H
authors.initials: H
authors.lastname: Kojima
authors.forename: H
authors.initials: H
authors.lastname: Moriyama
authors.forename: M
authors.initials: M
authors.lastname: Okabe
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D064032:Calbindin 2; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D007381:Intermediate Filament Proteins / Q000378:metabolism; D051656:KCNQ Potassium Channels / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D016253:Microscopy, Immunoelectron; D009419:Nerve Tissue Proteins / Q000378:metabolism; D064231:Nestin; D009457:Neuroglia / Q000378:metabolism* / Q000648:ultrastructure; D009474:Neurons / Q000378:metabolism* / Q000648:ultrastructure; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D027161:Satellite Cells, Perineuronal / Q000378:metabolism* / Q000648:ultrastructure; D014404:Tubulin / Q000378:metabolism; D014722:Vestibule, Labyrinth / Q000166:cytology* / Q000378:metabolism; D000098854:Kcnj10 Channel
chemical_list: D064032:Calbindin 2; D007381:Intermediate Filament Proteins; D051656:KCNQ Potassium Channels; D000098854:Kcnj10 Channel; C492167:Kcnq4 protein, mouse; D009419:Nerve Tissue Proteins; C577485:Nes protein, mouse; D064231:Nestin; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; D064030:S100 Calcium Binding Protein G; D014404:Tubulin; C462941:beta3 tubulin, mouse