Skellett R A, Crist J R, Fallon M, Bobbin R P
Kresge Hearing Research Laboratory of the South, Department of Otorhinolaryngology and Biocommunication, Louisiana State University Medical Center, New Orleans 70112, USA.
Hear Res. 1995 Jul;87(1-2):41-8. doi: 10.1016/0378-5955(95)00076-g.
The application of caffeine to the bathing medium of isolated cochlear outer hair cells (OHCs) induces shortening of the cells (Slepecky et al., 1988). This study was designed to test the hypothesis that a 'smooth muscle-like' mechanism was responsible for the caffeine-induced shortening of OHCs as suggested by Slepecky et al. OHCs were isolated from guinea pig cochleae and length measurements were taken during various drug perfusions. Antagonists of the ryanodine receptor/Ca(2+)-induced Ca2+ release (CICR; tetracaine, ruthenium red, and ryanodine) failed to block the caffeine-induced shortening of the OHCs. Application of the Ca2+ ionophore A23187 caused cell length to increase. These results did not support this hypothesis and therefore, an osmotic mechanism was proposed.
将咖啡因应用于分离的耳蜗外毛细胞（OHCs）的浴液中会导致细胞缩短（斯莱佩茨基等人，1988年）。本研究旨在检验一个假设，即如斯莱佩茨基等人所提出的，一种“平滑肌样”机制是咖啡因诱导OHCs缩短的原因。从豚鼠耳蜗中分离出OHCs，并在各种药物灌注期间进行长度测量。兰尼碱受体/钙诱导的钙释放（CICR）的拮抗剂（丁卡因、钌红和兰尼碱）未能阻断咖啡因诱导的OHCs缩短。应用钙离子载体A23187导致细胞长度增加。这些结果不支持这一假设，因此，提出了一种渗透机制。
