■耳鸣和高音,可能是由听力损失引发的,可归因于听觉感知中的适应不良可塑性。然而,由于它们的共存,解开它们的神经机制证明是困难的。我们假设耳鸣的神经相关因素与低强度音调触发的神经活动有关,而高音与对中等和高强度音调的反应有关。
■为了检验这些假设,我们在大鼠创伤后2至8天进行了行为和电生理实验。
■在行为实验中,预脉冲和间隙抑制倾向于表现出不同的频率特性(尽管没有达到足够的统计水平),这表明暴露于创伤性音调会导致不同频率范围内的急性音高和耳鸣。当检查丘脑皮层受体层的听觉皮层时,我们观察到耳鸣症状与杂乱无章的音调图相关,通常以对低强度音调的反应为特征。在多单位活动(MUA)水平的皮层募集功能中发现了运动过度的神经相关性,但不在局部场电位(LFP)水平,响应中等和高强度的音调。从LFP到MUA的这种转变与单调性的丧失有关,表明抑制性突触的关键作用。
■因此,在创伤性音调暴露的急性症状中,我们的实验成功地解开了耳鸣和听觉皮层的丘脑皮层受体层的神经相关性。他们还认为耳鸣与中枢噪音有关,而高音与异常的增益控制有关。动物实验和临床研究之间的进一步相互作用将提供对神经机制的见解,耳鸣和高音的诊断和治疗,特别是在慢性症状的长期可塑性方面。
UNASSIGNED: Both tinnitus and hyperacusis, likely triggered by hearing loss, can be attributed to maladaptive plasticity in auditory perception. However, owing to their co-occurrence, disentangling their neural mechanisms proves difficult. We hypothesized that the neural correlates of tinnitus are associated with neural activities triggered by low-intensity tones, while hyperacusis is linked to responses to moderate- and high-intensity tones.
UNASSIGNED: To test these hypotheses, we conducted behavioral and electrophysiological experiments in rats 2 to 8 days after traumatic tone exposure.
UNASSIGNED: In the behavioral experiments, prepulse and gap inhibition tended to exhibit different frequency characteristics (although not reaching sufficient statistical levels), suggesting that exposure to traumatic tones led to acute symptoms of hyperacusis and tinnitus at different frequency ranges. When examining the auditory cortex at the thalamocortical recipient layer, we observed that tinnitus symptoms correlated with a disorganized tonotopic map, typically characterized by responses to low-intensity tones. Neural correlates of hyperacusis were found in the cortical recruitment function at the multi-unit activity (MUA) level, but not at the local field potential (LFP) level, in response to moderate- and high-intensity tones. This shift from LFP to MUA was associated with a loss of monotonicity, suggesting a crucial role for inhibitory synapses.
UNASSIGNED: Thus, in acute symptoms of traumatic tone exposure, our experiments successfully disentangled the neural correlates of tinnitus and hyperacusis at the thalamocortical recipient layer of the auditory cortex. They also suggested that tinnitus is linked to central noise, whereas hyperacusis is associated with aberrant gain control. Further interactions between animal experiments and clinical studies will offer insights into neural mechanisms, diagnosis and treatments of tinnitus and hyperacusis, specifically in terms of long-term plasticity of chronic symptoms.