Adelman Cahtia, Weinberger Jeffrey M, Sohmer Haim
Speech & Hearing Center, Institute for Medical Research - Israel-Canada, Hebrew University-Hadassah Medical School, Jerusalem.
J Basic Clin Physiol Pharmacol. 2010;21(3):231-40. doi: 10.1515/jbcpp.2010.21.3.231.
The present study was designed to assess whether, in the presence of a depression of the cochlear amplifier i.e. a sensorineural hearing loss (SNHL), the inner hair cells (IHCs) require the presence of a normal endocochlear potential for transduction. An SNHL was induced by injecting salicylic acid (which binds to the motor protein prestin in the outer hair cells), and then furosemide (which depresses the endocochlear potential) was injected. Furosemide did not cause an additional elevation of the threshold of the auditory nerve brainstem evoked response (ABR) over that induced by the salicylic acid injection. Exposure to noise was also used to induce a SNHL in other mice, and then furosemide was injected. Here too furosemide did not cause an additional ABR threshold elevation over that induced by the noise. These results show that the IHCs (and the auditory nerve) can be excited in the presence of a SNHL (i.e. without the cochlear amplifier) and in the absence of an endocochlear potential. Possible mechanisms of excitation in such a state are discussed.
本研究旨在评估在耳蜗放大器功能降低即感音神经性听力损失（SNHL）的情况下，内毛细胞（IHC）进行转导是否需要正常的内淋巴电位。通过注射水杨酸（其与外毛细胞中的马达蛋白prestin结合）诱导SNHL，然后注射呋塞米（其降低内淋巴电位）。呋塞米并未使听神经脑干诱发电位（ABR）阈值在水杨酸注射所诱导的基础上进一步升高。暴露于噪声也被用于在其他小鼠中诱导SNHL，然后注射呋塞米。在此情况下，呋塞米同样未使ABR阈值在噪声所诱导的基础上进一步升高。这些结果表明，在存在SNHL（即没有耳蜗放大器）且不存在内淋巴电位的情况下，IHC（以及听神经）仍可被兴奋。文中讨论了在这种状态下兴奋的可能机制。
