Ca(2+) regulation of endocochlear potential in marginal cells.
We examined the effect of the cytosolic Ca(2+) concentration ([Ca(2+)](c)) in marginal cells on the asphyxia- or furosemide-induced decrease in the endocochlear potential (EP) by perfusing the endolymph with or without a Ca(2+) chelator or inhibitors of Ca(2+)-permeable channels or Ca(2+)-pump during transient asphyxia or intravenous administration of furosemide. We obtained the following results. (1) Endolymphatic administration of SKF96365 (an inhibitor of TRPC and L-type Ca(2+) channels) or EGTA-acetoxymethyl ester (EGTA-AM) significantly inhibited both the transient asphyxia-induced decrease in EP (TAID) and the furosemide-induced decrease in EP (FUID). (2) Endolymphatic perfusion with nifedipine significantly inhibited the TAID but not the FUID. (3) The recovery from the FUID was significantly suppressed by perfusing the endolymph with EGTA-AM, nifedipine, or SKF96365. (4) Endolymphatic administration of thapsigargin inhibited both the FUID and TAID. (5) The recovery rate from the FUID was much slower than that from the TAID, indicating that furosemide may inhibit the Ca(2+)-pump. (6) A strong reaction in immunohistochemical staining for TRPC channels was observed in the luminal and basolateral membranes of marginal cells. (7) A positive staining reaction for the gamma subunit of epithelial Na(+) channels was observed in the luminal and basolateral membranes of marginal cells. (8) Positive EP was diminished toward 0 mV by the endolymphatic perfusion with 10 muM amiloride or 10 muM phenamil. Taken together, these findings suggest that [Ca(2+)](c) regulated by endoplasmic Ca(2+)-pump and Ca(2+)-permeable channels in marginal cells may regulate the positive EP, which is partly produced by the diffusion potential of Na(+) across the basolateral membrane in marginal cells.
Mori
Yoshiaki
Y
Department of Physiology II, Osaka Medical College, 2-7 Daigakumachi, Takatsuki, Osaka, 569-8686, Japan.
Watanabe
Masahito
M
Inui
Takaki
T
Nimura
Yoshitsugu
Y
Araki
Michitoshi
M
Miyamoto
Manabu
M
Takenaka
Hiroshi
H
Kubota
Takahiro
T
D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D003051:Cochlea / Q000187:drug effects / Q000502:physiology*; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004710:Endolymph / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D053503:Epithelial Sodium Channels / Q000187:drug effects / Q000502:physiology; D005072:Evoked Potentials, Auditory / Q000187:drug effects / Q000502:physiology*; D005665:Furosemide / Q000494:pharmacology; D006168:Guinea Pigs; D007093:Imidazoles / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D026941:Sodium Channel Blockers / Q000494:pharmacology; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000494:pharmacology; D050052:TRPC Cation Channels / Q000187:drug effects / Q000502:physiology; D019284:Thapsigargin / Q000494:pharmacology
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D053503:Epithelial Sodium Channels; D007093:Imidazoles; D026941:Sodium Channel Blockers; D049994:Sodium Potassium Chloride Symporter Inhibitors; D050052:TRPC Cation Channels; C047088:phenylamil; D004533:Egtazic Acid; D019284:Thapsigargin; D000584:Amiloride; D005665:Furosemide; C046770:EGTA acetoxymethyl ester; C063159:1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; D009543:Nifedipine; D002118:Calcium