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外毛细胞延迟缩短和收缩过程中氯离子电导的调节

Regulation of Cl- conductance in delayed shortening and shrinkage of outer hair cells.

作者信息

Ohnishi S, Hara M, Inagaki C, Yamashita T, Kumazawa T

机构信息

Department of Otolaryngology, Kansai Medical University, Osaka, Japan.

出版信息

Acta Otolaryngol Suppl. 1993;500:42-5. doi: 10.3109/00016489309126177.

Abstract

Tetanic electrical field stimulation induces slow and delayed shortening of isolated outer hair cells (OHCs) from guinea pigs concomitant with a decrease in cell volume and intracellular Cl- concentration ([Cl-]i). These responses are dependent on the entry of Ca2+ and the activation of both Ca(2+)-activated K+ channels and furosemide-sensitive Cl- channels. In this study, the regulatory mechanisms of the Cl- channels of OHCs were investigated. Tetanic stimulation induced shrinkage and a decrease in [Cl-]i, the latter being unrelated to the activity of the Na+/K+/2Cl- cotransporter. These responses were inhibited by tetraethylammonium, and the inhibition was overcome by an increase in the K+ conductance by valinomycin, though valinomycin alone did not affect the resting cell volume and [Cl-]i. The deprivation of extracellular Ca2+ inhibited the stimulation-induced changes in volume and [Cl-]i even in the presence of valinomycin. These results suggest that electrical stimulation-induced delayed shortening and shrinkage of OHCs are induced by Cl- efflux, which is electrically coupled to K+ efflux and independently activated following an increase in intracellular Ca2+ concentration.

摘要

强直电场刺激可诱导豚鼠离体外毛细胞(OHC)缓慢且延迟的缩短,同时细胞体积和细胞内氯离子浓度([Cl-]i)降低。这些反应依赖于Ca2+的进入以及Ca(2+)-激活的K+通道和呋塞米敏感的Cl-通道的激活。在本研究中,对OHC的Cl-通道的调节机制进行了研究。强直刺激诱导细胞收缩和[Cl-]i降低,后者与Na+/K+/2Cl-共转运体的活性无关。这些反应被四乙铵抑制,并且通过缬氨霉素增加K+电导可克服这种抑制,尽管单独使用缬氨霉素并不影响静息细胞体积和[Cl-]i。细胞外Ca2+的剥夺即使在存在缬氨霉素的情况下也会抑制刺激诱导的体积和[Cl-]i变化。这些结果表明,电刺激诱导的OHC延迟缩短和收缩是由Cl-外流引起的,Cl-外流与K+外流电偶联,并在细胞内Ca2+浓度升高后独立激活。

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