title: Physiological role of L-type Ca2+ channels in marginal cells in the stria vascularis of guinea pigs.
abstract: Using immunohistochemical and electrophysiological methods, we investigated the role of L-type Ca(2+) channels in the regulation of the endocochlear potential (EP) of the endolymphatic surface cells (ESC) of the guinea pig stria vascularis. The following findings were made: (1) Administration of 30 microg/ml nifedipine via a vertebral artery significantly suppressed the transient asphyxia-induced decrease in the EP (TAID) and the transient asphyxia-induced increase in the Ca(2+), referred to as TAIICa, concentration in the endolymph ([Ca](e)). (2) The endolymphatic administration of 1 microg/ml nifedipine significantly inhibited the TAID as well as the TAIICa. The endolymphatic administration of nifedipine (0.001-10 microg/ml) inhibited the TAID in a dose-dependent manner. (3) The endolymphatic administration of (+)-Bay K8644, an L-type Ca(2+) channel closer, significantly inhibited the TAID, whereas (-)-Bay K8644, an L-type Ca(2+) channel opener, caused a large decrease in the EP from approximately +75 mV to approximately +20 mV at 10 min after the endolymphatic administration. (4) By means of immunohistochemistry, a positive staining reaction with L-type Ca(2+) channels was detected in the marginal cells of the stria vascularis. (5) Under the high [Ca](e) condition, we examined the mechanism of the TAIICa and hypothesized that the TAIICa might have been caused by the decrease in the EP through a shunt pathway in the ESC. (6) The administration of nifedipine to the endolymph significantly inhibited the Ba(2+)-induced decrease in the EP. These findings support the view that L-type Ca(2+) channels in the marginal cells regulate the EP, but not directly the TAIICa.
authors.affiliation: Department of Otolaryngology, Osaka Medical College, Takatsuki, Osaka, 569-8686, Japan.
authors.forename: Takaki
authors.initials: T
authors.lastname: Inui
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Mori
authors.forename: Masahito
authors.initials: M
authors.lastname: Watanabe
authors.forename: Atsuko
authors.initials: A
authors.lastname: Takamaki
authors.forename: Junko
authors.initials: J
authors.lastname: Yamaji
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Sohma
authors.forename: Ryotaro
authors.initials: R
authors.lastname: Yoshida
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takenaka
authors.forename: Takahiro
authors.initials: T
authors.lastname: Kubota
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D001237:Asphyxia / Q000503:physiopathology; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004710:Endolymph / Q000502:physiology*; D006168:Guinea Pigs; D007150:Immunohistochemistry; D017736:Ion-Selective Electrodes; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008839:Microelectrodes; D013316:Stria Vascularis / Q000187:drug effects / Q000502:physiology*
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D001464:Barium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D002118:Calcium