Auditory and non-auditory factors involved in loudness modulation: A model for tinnitus and hyperacusis

响度是声音的主要感知属性之一，是人们对声级的主观感受。虽然响度与声级之间的一般关系是单调的，但响度函数的细节可以根据若干听觉和非听觉因素而变化。例如，诸如感觉输入的减少和声音丰富的声学条件可以分别增加和降低听觉灵敏度。听觉系统具有根据周围听觉因素来调制增益的能力。然而，这个中心增益模型是一个最近的命题，并没有得到太多的实证支持。虽然已经提出脑干机制可能参与中枢增益调制，但尚不清楚是否更高水平的听觉系统也可能参与其中。在第一部分（听觉因素）中，我们将使用声音剥夺（耳塞）和丰富（噪声发生器）来研究剥夺/丰富的持续时间和强度，右侧/左侧暴露以及与年龄相关的听力损失对响度调制的影响。年轻和年长的参与者将佩戴耳塞或噪音发生器一周，并从周边进行听力测量（例如，自发耳声发射）到皮层（例如，磁长潜伏期听觉反应）将在该操作之前和之后进行。 在第二部分（非听觉因素）中，我们将研究压力对响度调制的作用。最近的一些研究（其中一些来自我们的实验室）已经揭示了压力和响度干扰之间的强关联，但没有数据可用于正常听力的响度调制中的压力的影响。我们将首先研究心理社会压力和合成皮质醇如何改变响度，并期望其中任何一种都能增加对声音的敏感性。接下来，我们将使用与第一部分类似的协议来检查心理社会压力/皮质醇和声音剥夺/丰富对响度的综合影响。 最后，在第三部分中，我们提出通过经颅直流电刺激来调节皮质兴奋性，这是一种无痛和安全的神经调节技术。预期皮层兴奋性的调制会改变听到幻声的概率，以及改变响度增长函数，其中每一个分别是耳鸣和听觉过敏的相关模型。 依靠我实验室开发的独特专业知识，这项研究计划将提供表征中枢增益机制的新证据，这是解释响度干扰的最新假设。此外，确定如何中央增益可以调制的压力将提供新的假设听觉和非听觉因素的相互作用，在正常的听觉功能和其修改的老化。

Loudness, the subjective perception of sound level (dB), is one of the major perceptual attributes of sounds. While the general relationship between loudness and sound level is monotonic, the details of the loudness function can vary depending on several auditory and non-auditory factors. For instance, acoustic conditions such as reduction of sensory inputs and sound enrichment can increase and decrease auditory sensitivity, respectively. The auditory system has the capacity to modulate the gain depending on ambient auditory factors. This central gain model, however, is a recent proposition that has not received much empirical support. While it has been suggested that brainstem mechanisms may be involved in central gain modulation, it is unknown whether higher levels of the auditory system may also participate. In PART I (Auditory factors) we will use sound deprivation (earplugs) and enrichment (noise generators) to investigate the influence of the duration and intensity of deprivation/enrichment, right/left sided exposure, and age-related hearing loss on loudness modulation. Groups of young and older participants will wear either earplugs or noise generators for one week, and hearing measures from periphery (e.g., spontaneous otoacoustic emissions) to cortex (e.g., magnetic long latency auditory responses) will be taken before and after this manipulation.  In PART II (Non-auditory factors) we will investigate the role of stress on loudness modulation. A few recent studies (some of which from our laboratory) have revealed strong associations between stress and loudness disturbances, but no data are available concerning the influence of stress in loudness modulation in normal hearing. We will first examine how psychosocial stress and synthetic cortisol alter loudness, with the expectation that either one can increase sensitivity to sounds. Next, we will examine the combined effect of psychosocial stress/cortisol and sound deprivation/enrichment on loudness, using protocols similar as in PART I.  Finally, in PART III we propose to modulate cortical excitability by transcranial direct current stimulation, a painless and safe neuromodulation technique. Modulation of cortical excitability is expected to change the probability of hearing phantom sounds, as well as change loudness growth functions, each of which being a relevant model of tinnitus and hyperacusis, respectively.  Relying on a unique expertise developed in my laboratory, this research program will provide novel evidence characterizing central gain mechanisms, the most recent hypothesis to explain loudness disturbances. In addition, determining how central gain can be modulated by stress will provide new hypotheses concerning auditory and non-auditory factor interaction in normal auditory function and its modification by aging.