Frolenkov G I, Belyantseva I A, Kurc M, Mastroianni M A, Kachar B
Section on Structural Cell Biology, Laboratory of Cellular Biology, NIDCD-NIH, Bethesda, MD 20852-3320, USA.
Hear Res. 1998 Dec;126(1-2):67-74. doi: 10.1016/s0378-5955(98)00150-6.
It is generally believed that the force for the otoacoustic emission (OAE) generation is provided by a mechanism of electromotility, observed in isolated cochlear outer hair cells (OHCs). OHC electromotility is resistant to several ototoxic reagents, it does not depend on ATP hydrolysis, but it can be blocked by specific sulfhydryl reagents: p-chloromercuriphenylsulfonic acid (pCMPS) and p-hydroxymercuriphenylsulfonic acid (pHMPS). We have used these reagents to test whether they also affect OAE. Application of pCMPS and pHMPS on the round window membrane of anesthetized guinea pigs produced a dose-dependent inhibition of the cubic (2F1-F2) distortion product OAE (DPOAE). The inhibition developed progressively from high to low frequencies, reflecting the diffusion of the drugs through the cochlear compartment. The effect of pCMPS and pHMPS was different from the effects of furosemide and lethal anoxia, which impair cochlear function but do not block OHC electromotility. pHMPS suppressed DPOAE completely at all sound intensities tested (45-80 dB SPL), whereas furosemide or lethal anoxia caused DPOAE to disappear at low-level stimulation (45-60 dB SPL) only. Our results suggest that the OHC electromotility might provide the force for DPOAE generation not only at low, but also at high stimulus intensities.
一般认为，耳声发射（OAE）产生的力量由在分离的耳蜗外毛细胞（OHC）中观察到的电运动机制提供。OHC电运动对几种耳毒性试剂具有抗性，它不依赖于ATP水解，但可被特定的巯基试剂阻断：对氯汞苯磺酸（pCMPS）和对羟基汞苯磺酸（pHMPS）。我们使用这些试剂来测试它们是否也会影响OAE。将pCMPS和pHMPS应用于麻醉豚鼠的圆窗膜会产生剂量依赖性的立方（2F1 - F2）畸变产物耳声发射（DPOAE）抑制。抑制作用从高频逐渐发展到低频，反映了药物在耳蜗隔室中的扩散。pCMPS和pHMPS的作用不同于速尿和致死性缺氧的作用，后者损害耳蜗功能但不阻断OHC电运动。在所有测试的声强（45 - 80 dB SPL）下，pHMPS完全抑制DPOAE，而速尿或致死性缺氧仅在低水平刺激（45 - 60 dB SPL）时导致DPOAE消失。我们的结果表明，OHC电运动可能不仅在低刺激强度下，而且在高刺激强度下都为DPOAE的产生提供力量。
