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A spiking neuron model of cortical correlates of sensorineural hearing loss: Spontaneous firing, synchrony, and tinnitus

机译:感觉神经性听力损失的皮质相关性的尖峰神经元模型:自发放电,同步性和耳鸣

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Hearing loss due to peripheral damage is associated with cochlear hair cell damage or loss and some retrograde degeneration of auditory nerve fibers. Surviving auditory nerve fibers in the impaired region exhibit elevated and broadened frequency tuning, and the cochleotopic representation of broadband stimuli such as speech is distorted. In impaired cortical regions, increased tuning to frequencies near the edge of the hearing loss coupled with increased spontaneous and synchronous firing is observed. Tinnitus, an auditory percept in the absence of sensory input, may arise under these circumstances as a result of plastic reorganization in the auditory cortex. We present a spiking neuron model of auditory cortex that captures several key features of cortical organization. A key assumption in the model is that in response to reduced afferent excitatory input in the damaged region, a compensatory change in the connection strengths of lateral excitatory and inhibitory connections occurs. These changes allow the model to capture some of the cortical correlates of sensorineural hearing loss, including changes in spontaneous firing and synchrony; these phenomena may explain central tinnitus. This model may also be useful for evaluating procedures designed to segregate synchronous activity underlying tinnitus and for evaluating adaptive hearing devices that compensate for selective hearing loss.
机译:周围神经损伤引起的听力丧失与耳蜗毛细胞损伤或丧失以及听觉神经纤维的某些逆行变性有关。受损区域中幸存的听觉神经纤维表现出升高的和增宽的频率调谐,并且宽带刺激(如语音)的耳蜗代表失真。在受损的皮层区域中,观察到对听力损失边缘附近频率的调谐增加,并伴有自发性和同步放电。在这种情况下,由于听觉皮层中的塑料重组,可能会出现耳鸣,即没有感觉输入的听觉。我们提出了一个尖锐的听觉皮层神经元模型,该模型捕获了皮质组织的几个关键特征。该模型中的一个关键假设是,响应于受损区域传入的兴奋性输入减少,横向兴奋性连接和抑制性连接的连接强度会发生补偿性变化。这些变化使模型能够捕获感觉神经性听力损失的一些皮质相关性,包括自发放电和同步性的变化。这些现象可能解释了中央耳鸣。该模型还可用于评估旨在隔离耳鸣下方的同步活动的过程,以及评估补偿选择性听力损失的自适应听力设备。

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