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

响度，即对声级的主观感知，是声音的主要感知属性之一。虽然响度和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几个听觉和非听觉因素而变化。例如，减少感觉输入和丰富声音等声学条件分别会增加和降低听觉敏感度。听觉系统具有根据环境听觉因素调节增益的能力。然而，这个核心收益模型是最近提出的一个命题，并没有得到太多的经验支持。虽然有人认为脑干机制可能涉及中枢增益调节，但尚不清楚听觉系统的更高水平是否也参与其中。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/左侧暴露以及年龄相关性听力损失对响度调制的影响。一组年轻的和年长的参与者将戴上耳塞或噪声发生器一周，并将在操作前后进行从外周(例如自发耳声发射)到皮质(例如磁性长潜伏期听觉反应)的听力测量。在第二部分(非听觉因素)中，我们将研究应激在响度调节中的作用。最近的一些研究(其中一些来自我们的实验室)揭示了应激和响度干扰之间的强烈联系，但没有关于应激对正常听力中响度调节的影响的数据。我们将首先研究心理社会压力和合成皮质醇是如何改变响度的，期望两者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方案，研究心理社会压力/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，我们建议通过经颅直流电刺激来调节皮质兴奋性，这是一种无痛且安全的神经调节技术。大脑皮层兴奋性的调节有望改变听觉幻听的概率，以及改变响度增长函数，每一个函数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，该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说。此外，确定中枢增益是如何被应激调节的，将为正常听觉功能中的听觉和非听觉因素的相互作用及其随年龄的变化提供新的假说。**

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. **