Wu Calvin, Martel David T, Shore Susan E
Kresge Hearing Research Institute, Department of Otolaryngology, and.
Kresge Hearing Research Institute, Department of Otolaryngology, and Departments of Biomedical Engineering and.
J Neurosci. 2016 Feb 10;36(6):2068-73. doi: 10.1523/JNEUROSCI.3960-15.2016.
Tinnitus, the perception of phantom sounds, is thought to arise from increased neural synchrony, which facilitates perceptual binding and creates salient sensory features in the absence of physical stimuli. In the auditory cortex, increased spontaneous cross-unit synchrony and single-unit bursting are de facto physiological correlates of tinnitus. However, it is unknown whether neurons in the dorsal cochlear nucleus (DCN), the putative tinnitus-induction site, exhibit increased synchrony. Using a temporary-threshold shift model and gap-prepulse inhibition of the acoustic startle to assess tinnitus, we recorded spontaneous activity from fusiform cells, the principle neurons of the DCN, in normal hearing, tinnitus, and non-tinnitus guinea pigs. Synchrony and bursting, as well as spontaneous firing rate (SFR), correlated with behavioral evidence of tinnitus, and increased synchrony and bursting were associated with SFR elevation. The presence of increased synchrony and bursting in DCN fusiform cells suggests that a neural code for phantom sounds emerges in this brainstem location and likely contributes to the formation of the tinnitus percept.
Tinnitus, a phantom auditory percept, is encoded by pathological changes in the neural synchrony code of perceptual processing. Increased cross-unit synchrony and bursting have been linked to tinnitus in several higher auditory stations but not in fusiform cells of the dorsal cochlear nucleus (DCN), key brainstem neurons in tinnitus generation. Here, we demonstrate increased synchrony and bursting of fusiform cell spontaneous firing, which correlate with frequency-specific behavioral measures of tinnitus. Thus, the neural representation of tinnitus emerges early in auditory processing and likely drives its pathophysiology in higher structures.
耳鸣，即对幻听的感知，被认为源于神经同步性增加，这种同步性促进了感知整合，并在没有物理刺激的情况下产生显著的感觉特征。在听觉皮层，自发跨单元同步性增加和单单元爆发实际上是耳鸣的生理相关指标。然而，尚不清楚作为假定耳鸣诱导部位的背侧耳蜗核（DCN）中的神经元是否表现出同步性增加。我们使用临时阈移模型和听觉惊吓的间隙前脉冲抑制来评估耳鸣，记录了正常听力、耳鸣和非耳鸣豚鼠中DCN的主要神经元梭形细胞的自发活动。同步性、爆发以及自发放电率（SFR）与耳鸣的行为证据相关，同步性和爆发增加与SFR升高有关。DCN梭形细胞中同步性和爆发增加表明，在这个脑干位置出现了幻听的神经编码，并且可能有助于耳鸣感知的形成。
耳鸣，一种幻听感知，由感知处理的神经同步编码中的病理变化编码。跨单元同步性增加和爆发与几个高级听觉中枢的耳鸣有关，但与背侧耳蜗核（DCN）的梭形细胞无关，DCN是耳鸣产生中的关键脑干神经元。在这里，我们证明了梭形细胞自发放电的同步性和爆发增加，这与耳鸣的频率特异性行为指标相关。因此，耳鸣的神经表征在听觉处理早期出现，并可能驱动其在高级结构中的病理生理学。
