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The pattern of vestibular nerve response to loud sound after total destruction of cochlea

耳蜗完全破坏后前庭神经对大声的反应模式

基本信息

批准号：
15591836
负责人：
OCHI Kentaro
金额：
$ 2.3万
依托单位：
St.Marianna University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15591836/
关键词：
cochlear destruction vestibular nerve single unit amikacin loud sound vestibular evoked myogenic potential 前庭性誘発筋電位音響外傷

项目摘要

The purpose of this study was to examine the underlying mechanisms of vestibular evoked myogenic potential(VEMP) by performing single unit recording from vestibular nerve in response to the loud sound after total destruction of cochlea Firstly, we tried to destruct cochlea by administration of aminoglycoside. One month after intramuscularly administration of amikacin at the dose 450 mg/kg for 14 days, action potential was still recorded. Then we increased dosage from 450 mg/kg to 900 mg/kg. The cochlea was completely destructed after 1 month, however acoustic stimuli induced no response at the maximum sound intensity. This suggests that the administration of amikacine induced destruction not only cochlea but also vestibule. We tried to determine the appropriate dosage which destruct cochlea without destruct vestibule. Although we applied two additional dosages of 450 mg/kg and 700 mg/kg, we failed to decide appropriate dosage.Secondary, we tried to destruct cochlea by loud sound. Animals were exposed to the white noise at the intensity of 115 dB for 12hours, compound action potential was still recorded and this suggests that the cochlea was not destructed. Thirdly, we evaluated the effects of tinnitus inducing drugs (salicylate and quinine) on both cochlea and auditory cortex. Either intra-venous administration of salicylate or intramuscular administration of quinine induced no marked change in spontaneous activity in the primary auditory cortex. The effects of drugs on the spontaneous activity in the cochlear nerve were not confirmed. We reported the changes in CAP adaptation in experimentally induced endolymphatic hydrops.We also performed clinical study and reported the VEMP pattern who suffered from Ramsay Hunt syndrome, acute sensorineural hearing loss, vestibular neuritis, and narrow internal auditory canal. In addition, the effect of age on VEMP was reported.

本研究的目的是探讨前庭诱发肌源性电位（VEMP）的机制。首先，我们尝试用氨基糖苷类药物损毁耳蜗，然后用单单位记录法记录前庭神经对强声刺激的反应。肌肉注射阿米卡星450 mg/kg 14 d后1个月，仍记录到动作电位。然后我们将剂量从450 mg/kg增加到900 mg/kg。1个月后耳蜗完全破坏，但在最大声强下声刺激未引起反应。提示丁胺卡那不仅对耳蜗有破坏作用，而且对前庭也有破坏作用。我们试图确定在不破坏前庭的情况下破坏耳蜗的合适剂量。虽然我们追加了450 mg/kg和700 mg/kg两个剂量，但未能确定合适的剂量。将动物暴露于强度为115 dB的白色噪声中12 h，仍能记录到复合动作电位，提示耳蜗未受到破坏。第三，我们评估了耳鸣诱导药物水杨酸和奎宁对耳蜗和听皮层的影响。无论是静脉注射水杨酸盐或肌肉注射奎宁引起的自发活动在初级听觉皮层没有显着的变化。药物对耳蜗神经自发活动的影响尚未得到证实。本文报道了实验性内淋巴积水的CAP适应性改变，并对Ramsay Hunt综合征、急性感音神经性聋、前庭神经炎、内听道狭窄患者的VEMP模式进行了临床研究。此外，还报告了年龄对VEMP的影响。