Synaptopathy and Neural Gain Following Low-Level Noise Exposure

项目摘要/摘要 长时间低水平(LDLL)噪声暴露可增强或抑制声音诱发的活动 听觉皮质(AC)，但尚不清楚这些神经可塑性变化是起源于AC还是遗传自 听觉通路的较低水平。为了解决这个问题，录音将从耳蜗处获得，下级 确定丘脑(IC)和AC的变化幅度和方向。要确定LDLL噪声是否 暴露扰乱了中枢听觉通路的神经输入，我们将评估内毛细胞 突触后I型传入纤维上表达的突触带和关键蛋白。我们的工作假说 低密度脂蛋白噪声暴露会抑制耳蜗神经输出，但中枢听觉通路 通过在听觉通路的逐渐更高的水平上增强神经增益来补偿这一点。

Project Summary/Abstract Long-duration low-level (LDLL) noise exposures can enhance or depress sound-evoked activity in the auditory cortex (AC), but it’s unclear if these neuroplastic changes originate in the AC or are inherited from lower levels of the auditory pathway. To address this, recordings will be obtained from the cochlea, inferior colliculus (IC) and AC to determine the magnitude and direction of change. To determine if LDLL noise exposures disrupt the neural input to the central auditory pathway, we will evaluate the inner hair cell pre- synaptic ribbons and key proteins expressed on the post-synaptic type I afferent fibers. Our working hypothesis is LDLL noise exposure depresses the neural output of the cochlea, but the central auditory pathway compensates for this by enhancing neural gain at progressively higher levels of the auditory pathway.