Tinnitus is one of the most prevalent auditory disorders worldwide, manifesting in both chronic and acute forms. The pathology of tinnitus has been mechanistically linked to induction of harmful neural plasticity stemming from traumatic noise exposure, exposure to ototoxic medications, input deprivation from age-related hearing loss, and in response to injuries or disorders damaging the conductive apparatus of the ears, the cochlear hair cells, the ganglionic cells of the VIIIth cranial nerve, or neurons of the classical auditory pathway which link the cochlear nuclei through the inferior colliculi and medial geniculate nuclei to auditory cortices. Research attempting to more specifically characterize the neural plasticity occurring in tinnitus have used a wide range of techniques, experimental paradigms, and sampled at different windows of time to reach different conclusions about why and which specific brain regions are crucial in the induction or ongoing maintenance of tinnitus-related plasticity. Despite differences in experimental methodologies, evidence reveals similar findings that strongly suggest that immediate and prolonged activation of non-classical auditory structures (i.e., amygdala, hippocampus, and cingulate cortex) may contribute to the initiation and development of tinnitus in addition to the ongoing maintenance of this devastating condition. The overarching focus of this review, therefore, is to highlight findings from the field supporting the hypothesis that abnormal early activation of non-classical sensory limbic regions are involved in tinnitus induction, with activation of these regions continuing to occur at different temporal stages. Since initial/early stages of tinnitus are difficult to control and to quantify in human clinical populations, a number of different animal paradigms have been developed and assessed in experimental investigations. Reviews of traumatic noise exposure and ototoxic doses of sodium salicylate, the most prevalently used animal models to induce experimental tinnitus, indicate early limbic system plasticity (within hours, minutes, or days after initial insult), supports subsequent plasticity in other auditory regions, and contributes to the pathophysiology of tinnitus. Understanding this early plasticity presents additional opportunities for intervention to reduce or eliminate tinnitus from the human condition.

中文翻译：

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耳鸣实验模型早期边缘区域的可塑性

耳鸣是全世界最普遍的听觉障碍之一，有慢性和急性两种形式。耳鸣的病理学在机制上与由于创伤性噪音暴露、接触耳毒性药物、年龄相关性听力损失导致的输入剥夺以及对损伤耳朵传导装置的损伤或疾病的反应而诱发有害的神经可塑性有关。耳蜗毛细胞、第八脑神经的神经节细胞或经典听觉通路的神经元，通过下丘和内侧膝状核将耳蜗核连接到听觉皮层。试图更具体地描述耳鸣中发生的神经可塑性的研究使用了广泛的技术、实验范式，并在不同的时间窗口进行采样，以得出不同的结论，即为什么以及哪些特定的大脑区域对于耳鸣的诱导或持续维持至关重要。耳鸣相关的可塑性。尽管实验方法存在差异，但证据揭示了类似的发现，强烈表明非经典听觉结构（即杏仁核、海马体和扣带皮层）的立即和长期激活除了持续的维持之外可能有助于耳鸣的发生和发展。这种毁灭性的情况。因此，本次综述的首要重点是强调该领域的研究结果，支持以下假设：非经典感觉边缘区域的异常早期激活与耳鸣诱发有关，这些区域的激活在不同的时间阶段持续发生。由于耳鸣的初始/早期阶段在人类临床人群中难以控制和量化，因此在实验研究中开发和评估了许多不同的动物范例。对创伤性噪音暴露和水杨酸钠耳毒性剂量（最常用的诱导实验性耳鸣的动物模型）的审查表明早期边缘系统可塑性（初次损伤后数小时、数分钟或数天内），支持其他听觉区域的后续可塑性，并且有助于耳鸣的病理生理学。了解这种早期可塑性为减少或消除人类耳鸣的干预提供了额外的机会。