Brown M C, Nuttall A L, Masta R I, Lawrence M
Hear Res. 1983 Feb;9(2):131-44. doi: 10.1016/0378-5955(83)90023-0.
Intracellular potentials were recorded from inner hair cells in the guinea pig cochlea. Transient asphyxia was induced by interrupting respiration for brief periods. Asphyxia caused a hyperpolarization of the resting membrane potential (resting Em). The hyperpolarization averaged 2.9 mV for 30 s asphyxias and 5.7 mV for 45 s asphyxias. The membrane potential recovered quickly after normal ventilation was resumed. Asphyxia also induced a rapid and profound decrease of the d.c. receptor potential in response to moderate intensity tone bursts at the characteristic frequency of the inner hair cell. At maximal depression, the receptor potential was reduced about 60% for a 30 s asphyxia and 100% for a 45 s asphyxia. The receptor potential recovered slowly after normal ventilation was resumed. A similar percent reduction and time course of recovery were observed for the a.c. receptor potential. In recordings from the same animals, the round window compound action potential (CAP) was as severely depressed by asphyxia as the hair cell receptor potentials. The time course of recovery for the CAP was similar to the slow recovery of the d.c. receptor potential. In contrast, the round window cochlear microphonics (CM) and the endolymphatic potential (EP) were affected less by asphyxia and recovered quickly after ventilation was resumed. Frequency tuning curves (FTCs) for the d.c. receptor potential were measured during the period of maximal receptor potential depression. These FTCs showed decreased tip sensitivity and a decrease in sharpness of tuning, as measured by the Q10. These changes were fully reversible. Low frequency (tail) segments of the FTCs were much less affected by asphyxia. The inner hair cell FTC changes during asphyxia were compared with neural FTC changes reported by other investigators. The similarities lead us to the conclusion that the inner hair cell and the auditory neural response to sound are equally sensitive to asphyxia.
在豚鼠耳蜗的内毛细胞中记录细胞内电位。通过短暂中断呼吸诱导短暂性窒息。窒息导致静息膜电位(静息Em)超极化。30秒窒息时超极化平均为2.9毫伏,45秒窒息时为5.7毫伏。恢复正常通气后,膜电位迅速恢复。窒息还导致内毛细胞特征频率下中等强度短纯音诱发的直流受体电位迅速且显著降低。在最大抑制时,30秒窒息使受体电位降低约60%,45秒窒息使其降低100%。恢复正常通气后,受体电位恢复缓慢。交流受体电位也观察到类似的降低百分比和恢复时间进程。在同一动物的记录中,圆窗复合动作电位(CAP)与毛细胞受体电位一样受到窒息的严重抑制。CAP的恢复时间进程与直流受体电位的缓慢恢复相似。相比之下,圆窗耳蜗微音电位(CM)和内淋巴电位(EP)受窒息影响较小,通气恢复后迅速恢复。在受体电位最大抑制期间测量直流受体电位的频率调谐曲线(FTC)。这些FTC显示尖端敏感性降低,以Q10衡量的调谐锐度降低。这些变化是完全可逆的。FTC的低频(尾部)段受窒息影响小得多。将窒息期间内毛细胞FTC的变化与其他研究者报道的神经FTC变化进行比较。这些相似性使我们得出结论,内毛细胞和听觉神经对声音的反应对窒息同样敏感。