Cortical Mechanisms of Auditory-Vocal Interaction

听觉-声音相互作用的皮质机制

• 批准号: 9180693
• 负责人: STEVEN J ELIADES
• 金额: $ 23.48万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2014
• 资助国家: 美国
• 起止时间: 2014-12-01 至 2019-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9180693
• 关键词: Accelerometer; Acoustics; Address; Animal Experiments; Animal Vocalization; Animals; Area; Auditory; Auditory area; Brain; Brain region; Callithrix; Communication; Detection; Electric Stimulation; Epilepsy; Exhibits; Feedback; Financial compensation; Frequencies; Future; Goals; Hearing; Human; Impairment; Intractable Epilepsy; Lead; Learning; Measurement; Measures; Methods; Modeling; Monitor; Monkeys; Motor; Motor Cortex; Neural Pathways; Neurons; Operative Surgical Procedures; Patients; Play; Primates; Process; Production; Research; Role; Sensory; Signal Transduction; Site; Source; Speech; Speech Disorders; Testing; Translating; Translations; Voice; Work; experimental study; frontal lobe; hearing impairment; human subject; motor control; neuromechanism; neurophysiology; neurotransmission; nonhuman primate; novel strategies; public health relevance; relating to nervous system; response; sound; time use; vocal control; vocalization

DESCRIPTION (provided by applicant): The overall objective of this research is to understand how we listen to the sound of our own voice while talking and how we use this information to help control our speech. Humans have sophisticated mechanisms for self-monitoring of this vocal feedback during speech that allow for the detection and compensation for vocal errors. Degradation of this self-monitoring, such as following hearing loss, results in difficulty in acquiring and maintaining normal speech and impairs vocal communication. Recent work in both humans and primates has demonstrated a suppression of neural activity in the auditory cortex during vocalization that may play a role in self-monitoring. The origin and significance of this neural activity is unknown. This proposal focuses on determining the neural mechanism of self-monitoring during vocal production and its role in feedback vocal control, using both human subjects and a vocal primate model, the marmoset monkey. Aim 1 tests the hypothesis that suppressed neurons of the auditory cortex in marmosets exhibit self- monitoring activity, and that this neural activity can drive compensatory vocal control. Auditory cortex neurons are recorded from vocalizing marmosets while altering the frequency content of their vocal feedback to induce vocal compensation. Neural recording is followed by electrical stimulation of the auditory cortex in order to disrupt self-monitoring and resulting feedback compensation. These experiments will demonstrate how vocalization self-monitoring activity in the auditory cortex drives feedback vocal control. Aim 2 tests the hypothesis that frontal cortical areas, particularl pre-motor cortex, are the origin of the neural signals that cause vocal suppression in auditory cortex. Neurons in both frontal and auditory cortex of marmosets are recorded simultaneously and quantitative analyses applied to demonstrate neural connectivity between brain regions during vocal production. These results will demonstrate the neural pathways beyond auditory cortex that contribute to vocal self-monitoring. Aim 3 tests the hypothesis that human auditory cortex is necessary for self-monitoring and feedback vocal control of speech. Auditory cortex activity is recorded using intracranial electrocorticographic activity in patients undergoing neura monitoring for epilepsy surgery. Paralleling the animal experiments, electrical stimulation of cortex is performed during pitch-altered speech feedback to demonstrate the role of auditory cortex in feedback compensation. These experiments will have implications for understanding speech motor control and will allow mechanistic comparisons between human speech and animal vocalization. Such comparisons are critical as we attempt to translate results from animal neurophysiology towards understanding human speech production.

描述（由申请人提供）：这项研究的总体目标是了解我们如何在说话时倾听自己的声音，以及我们如何使用这些信息来帮助控制我们的言语。人类有复杂的机制来自我监测这种语音反馈，允许检测和补偿语音错误。这种自我监测的退化，例如听力损失，导致难以获得和维持正常的言语，并损害声音交流。最近对人类和灵长类动物的研究表明，在发声过程中，听觉皮层的神经活动受到抑制，这可能在自我监测中发挥作用。这种神经活动的起源和意义尚不清楚。这项建议的重点是确定在发声过程中自我监测的神经机制及其在反馈发声控制中的作用，使用人类受试者和发声灵长类动物模型，绒猴。 目的1验证绒猴听觉皮层受抑制的神经元表现出自我监控活动的假设，并且这种神经活动可以驱动补偿性发声控制。通过改变发声绒猴的声音反馈的频率成分来诱导发声补偿，从而记录到发声绒猴的听觉皮层神经元。神经记录之后是听觉皮层的电刺激，以破坏自我监控和由此产生的反馈补偿。这些实验将展示听觉皮层中的发声自我监控活动如何驱动反馈发声控制。 目的2：验证额叶皮层，特别是运动前区是听觉皮层中引起发声抑制的神经信号的来源这一假说。同时记录了绒猴额叶和听觉皮层的神经元，并应用定量分析来证明发声过程中大脑区域之间的神经连接。这些结果将证明听觉皮层以外的神经通路，有助于声乐自我监测。 目的3：验证人类听觉皮层对言语的自我监控和反馈发声控制是必要的这一假设。在癫痫手术中接受神经监测的患者中，使用颅内皮层电图活动记录听觉皮层活动。在动物实验的基础上，采用电刺激皮层的方法，研究了音高变化的言语反馈对听觉皮层的影响。这些实验将对理解言语运动控制产生影响，并将允许人类言语和动物发声之间的机械比较。当我们试图将动物神经生理学的结果转化为理解人类语言产生时，这种比较是至关重要的。