Kitano I, Mori N, Matsunaga T
Department of Otolaryngology, Nara Medical University, Japan.
Hear Res. 1995 Mar;83(1-2):37-42. doi: 10.1016/0378-5955(94)00187-u.
To determine the role of anion transport in the forskolin-induced Cl- increase of scala media (SM), effects of forskolin on the EP (endocochlear potential) and Cl- activity (ACl) in SM were examined with double-barrelled Cl(-)-selective microelectrodes. The experiments were carried out on guinea pig cochleae, using a few anion transport inhibitors: IAA-94 for a Cl- channel blocker, bumetanide (BU) for an Na+/K+/2Cl- cotransport blocker, and SITS and DIDS for Cl-/HCO3- exchange blockers. The application of forskolin (200 microM) into scala vestibuli (SV) caused a 20 mEq increase of endolymphatic ACl and a 15 mV elevation of EP, and IAA-94 with forskolin completely abolished these responses. Although each application of BU, SITS or DIDS did not completely suppress EP elevation, the concurrent application of these inhibitors completely suppressed EP with endolymphatic ACl increase. The results indicate the involvement of Cl- channels, Na+/K+/2Cl- cotransport and Cl-/HCO3- exchange in forskolin-induced increase of ACl and EP. The role of adenylate cyclase activation and Cl- transport in endolymph homeostasis was discussed.
为了确定阴离子转运在福司可林诱导的中阶（SM）氯离子增加中的作用，使用双管氯离子选择性微电极检测了福司可林对中阶内电位（EP）和氯离子活性（ACl）的影响。实验在豚鼠耳蜗上进行，使用了几种阴离子转运抑制剂：IAA - 94作为氯离子通道阻滞剂，布美他尼（BU）作为钠/钾/2氯离子协同转运阻滞剂，以及SITS和DIDS作为氯/碳酸氢根交换阻滞剂。将福司可林（200 microM）应用于前庭阶（SV）导致内淋巴ACl增加20 mEq，EP升高15 mV，而IAA - 94与福司可林一起完全消除了这些反应。虽然单独应用BU、SITS或DIDS并未完全抑制EP升高，但这些抑制剂同时应用可完全抑制EP升高及内淋巴ACl增加。结果表明氯离子通道、钠/钾/2氯离子协同转运和氯/碳酸氢根交换参与了福司可林诱导的ACl和EP增加。讨论了腺苷酸环化酶激活和氯离子转运在内淋巴稳态中的作用。
