The auditory system has an extensive efferent innervation, which contributes to processes of control and regulation of the afferent input. The expression of receptors to various neurotransmitters and neuropeptides in the inner ear has been described, among which endogenous opioid receptors are found. The role of opioid receptors in the cochlea is not yet fully defined, it has been reported that opioid agonists and antagonists modulate the response to auditory stimuli and in clinical practice, multiple cases have been reported in which the consumption of opioid derivatives induce sensorineural hearing loss. In this work, we evaluated the effects of acute treatment with morphine, fentanyl, tramadol, and naloxone, in the auditory brain stem potentials (ABR), the compound action potential (CAP), and distortion products otacoustic emissions (DPOAE), across a wide range of stimulus frequencies and amplitudes. Adult Long-Evans rats of the strain CII/ZV weighing 180-220 g were used. For the ABR recording drugs were administered intraperitoneally or intravenously. For the CAP and DPOAE drugs were applied by direct perfusion in the middle ear. The opioid agonists produced a consistent increase in the amplitude of the PI component of the ABR and of the N1-P1 amplitude of the CAP. Naloxone produced no significant changes in the ABR and a reduction of the CAP N1-P1 amplitude. Also, opioid agonists induced a decrease in the amplitude of the DPOAE. These results show that the opioid receptor activation modulates both the afferent response at both the afferent response to acoustic stimuli, and also at the cochlear mechanics as revealed by DPOAE changes. These results present a significant step in understanding how opioid modulation of auditory responses may contribute to the auditory processing and to sensorineural hearing loss produced by opioids.

中文翻译：

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大鼠内耳中耳蜗听觉反应的阿片样物质调节。

听觉系统具有广泛的传出神经，这有助于传入输入的控制和调节过程。已经描述了内耳中各种神经递质和神经肽受体的表达，其中发现了内源性阿片受体。阿片受体在耳蜗中的作用尚未完全确定，据报道，阿片激动剂和拮抗剂可调节对听觉刺激的反应，在临床实践中，已报道了多起服用阿片衍生物诱发感觉神经性听力损失的病例。 。在这项工作中，我们评估了吗啡，芬太尼，曲马多和纳洛酮急性治疗对听性脑干电位（ABR），复合动作电位（CAP）和畸变产物脉动排放（DPOAE）的影响，跨越各种刺激频率和振幅。使用重180-220g的CII / ZV毒株的成年Long-Evans大鼠。对于ABR记录药物，腹膜内或静脉内给药。对于CAP和DPOAE药物，通过在中耳直接灌注来应用。阿片类激动剂使ABR的PI成分的振幅和CAP的N1-P1振幅一致增加。纳洛酮在ABR中没有产生显着变化，并且CAP N1-P1振幅没有降低。而且，阿片样物质激动剂引起DPOAE幅度的降低。这些结果表明，阿片样物质受体激活既调节了对听觉刺激的传入反应，又调节了DPOAE变化揭示的耳蜗力学。