Neural Mechanisms of sound intensity coding

声强编码的神经机制

• 批准号: 8431681
• 负责人: KATRINA M MACLEOD
• 金额: $ 32.95万
• 依托单位: UNIV OF MARYLAND, COLLEGE PARK
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-03-01 至 2015-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8431681
• 关键词: Acoustic Nerve; Acoustics; Address; Animals; Area; Auditory; Birds; Brain; Brain Stem; Characteristics; Cochlear Implants; Cochlear nucleus; Code; Communication; Cues; Development; Devices; Electric Stimulation; Elements; Environment; Exhibits; Goals; Hearing; Human; In Vitro; Intervention; Investigation; Knowledge; Lead; Link; Maintenance; Measures; Mediating; Mental Depression; N-Methyl-D-Aspartate Receptors; Nerve; Nerve Fibers; Neural Pathways; Neuraxis; Neurons; Neurophysiology - biologic function; Output; Pathway interactions; Patients; Pattern; Physiological; Preparation; Presynaptic Terminals; Process; Property; Prosthesis; Research; Role; Sensory Process; Signal Transduction; Slice; Sound Localization; Speech; Staging; Stimulus; Synapses; Synaptic plasticity; System; Testing; Time; Training; Translating; Work; auditory pathway; base; hearing impairment; implantable device; improved; in vivo; insight; neuromechanism; neurophysiology; novel; postsynaptic; presynaptic; public health relevance; relating to nervous system; research study; response; restoration; sound; transmission process

DESCRIPTION (provided by applicant): A detailed understanding of the neurophysiological basis of hearing is fundamental to the understanding of human hearing impairment and the guidance of further development of the most successful prosthetic intervention to date, the cochlear implant. Yet we still lack a complete description of how sound information is processed at even the first central nervous system relay, the cochlear nucleus. Different aspects of sound are extracted from the auditory nerve spike trains and encoded via parallel neural pathways. While the coding of timing cues have been studied extensively, the processing of intensity cues remains unclear, especially relating to non-localization tasks such as sound recognition. We recently determined that the timing and intensity circuits in the cochlear nucleus are distinguished by the expression of different forms of short-term synaptic plasticity. In vitro studies have demonstrated that the intensity pathways exhibit a mixture of short-term facilitation and depression that allows the transmission of rate-encoded intensity information. In contrast, the short-term depression found in timing circuits creates a synaptic gain control that contributes to intensity-invariant coding of timing cues. We expand our investigation of intensity coding to spike trains in response to dynamic, amplitude modulated sounds, an important component of sound communication signals. The goal of this proposal is to identify the synaptic and cellular mechanisms that contribute to the encoding of sound intensity and establish their importance in the intact brain. Aim 1 uses the avian (chick) cochlear nucleus slice preparation to investigate two synaptic enhancement mechanisms: short-term synaptic facilitation and the contribution of NMDA-receptor currents to synaptic integration. We use dynamic clamp to determine the input-output function of cochlear nucleus neurons. Aim 2 investigates how dynamic stimuli like amplitude-modulated sounds are processed at auditory nerve synapses in the cochlear nucleus by measuring physiological synaptic responses to rate-modulated spike train inputs, using electrical stimulation and dynamic clamp. In Aim 3, we will extend our in vitro short-term plasticity results to the intact cochlear nucleus with in vivo, intracellular recordings in the avian brainstem. Given the recent advances in the restoration of hearing using prosthetic devices that stimulate the auditory nerve, it is critical to understand how nerve activity is interpreted by the central nervous system. This proposal will provide new information on the transformation of auditory information which will help improve assisted-hearing devices and lead to a better understanding of normal hearing.

描述（由申请人提供）：详细了解听力的神经生理学基础对于了解人类听力障碍和指导迄今为止最成功的人工干预（人工耳蜗植入）的进一步发展至关重要。然而，我们仍然缺乏一个完整的描述，如何声音信息是处理在甚至第一个中枢神经系统中继，耳蜗核。声音的不同方面是从听觉神经尖峰序列中提取的，并通过并行的神经通路进行编码。虽然时间线索的编码已被广泛研究，但强度线索的处理仍不清楚，特别是与非定位任务，如声音识别。我们最近确定，在耳蜗核的时间和强度电路的区别不同形式的短期突触可塑性的表达。体外研究表明，强度通路表现出短期易化和抑制的混合，允许速率编码的强度信息的传输。相比之下，在定时电路中发现的短期抑制产生了突触增益控制，有助于定时线索的强度不变编码。我们扩大我们的调查强度编码的尖峰列车响应动态，调幅的声音，声音通信信号的一个重要组成部分。这项计划的目标是确定有助于声音强度编码的突触和细胞机制，并确定它们在完整大脑中的重要性。目的1利用鸡耳蜗核薄片标本研究突触增强的两种机制：短时程突触易化和NMDA受体电流对突触整合的贡献。用动态钳夹法测定耳蜗核神经元的输入输出功能。目的2研究如何动态刺激，如调幅的声音是在耳蜗核听觉神经突触的处理，通过测量生理突触反应率调制的棘波序列输入，使用电刺激和动态钳。在目标3中，我们将扩展我们的体外短期可塑性的结果，完整的耳蜗核在体内，细胞内记录在鸟类脑干。鉴于最近在使用刺激听觉神经的假体设备恢复听力方面取得的进展，理解中枢神经系统如何解释神经活动至关重要。该提案将提供有关听觉信息转换的新信息，这将有助于改进辅助听力设备，并导致更好地理解正常听力。