K+ channel function in vestibular ganglion neurons

前庭神经节神经元的 K 通道功能

• 批准号: 7106236
• 负责人: JESSICA R RISNER
• 金额: $ 2.81万
• 依托单位: UNIVERSITY OF VIRGINIA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7106236
• 关键词: action potentials; ganglions; gene expression; green fluorescent proteins; immunocytochemistry; inhibitor /antagonist; laboratory mouse; messenger RNA; neuropharmacology; point mutation; polymerase chain reaction; potassium channel; predoctoral investigator; protein localization; protein structure function; tissue /cell culture; transfection /expression vector; vestibular nerve; voltage /patch clamp; voltage gated channel

DESCRIPTION (provided by applicant): Vestibular ganglion neurons convey information from the vestibular end organs to the brainstem. The neurons encode the onset, direction, frequency, magnitude and other aspects of vestibular stimuli. How that information is encoded has not yet been clarified. Preliminary data suggest a heterogeneous population of K+ conductances underlie the diverse firing properties of these neurons and affect how vestibular information is encoded. Understanding the physiological characteristics of vestibular ganglia K+ conductances will allow for a better understanding of how vestibular information is encoded and provide a rational basis for possible therapies to treat vestibular dysfunction. This project aims to study the role of K+ channels and their contribution to normal vestibular function with particular focus on KCNQ channels. Mutations in four out of the five KCNQ channels result in genetic disorders, including deafness and vestibular dysfunction. These experiments will examine the expression and contribution of KCNQ channels to the electrophysiological properties of vestibular ganglion neurons using a multidisciplinary approach, including immunohistochemistry, whole-cell recording, pharmacology, and dominant-negative channel suppression.

描述（由申请人提供）：前庭神经节神经元将信息从前庭终末器官传递到脑干。神经元对前庭刺激的开始、方向、频率、幅度和其他方面进行编码。该信息如何编码尚未明确。初步数据表明，K+电导的异质群体是这些神经元不同放电特性的基础，并影响前庭信息的编码方式。了解前庭神经节 K+ 电导的生理特征将有助于更好地理解前庭信息的编码方式，并为治疗前庭功能障碍的可能疗法提供合理的基础。该项目旨在研究 K+ 通道的作用及其对正常前庭功能的贡献，特别关注 KCNQ 通道。五个 KCNQ 通道中的四个突变会导致遗传性疾病，包括耳聋和前庭功能障碍。这些实验将使用多学科方法（包括免疫组织化学、全细胞记录、药理学和显性负性通道抑制）检查 KCNQ 通道的表达和对前庭神经节神经元电生理特性的贡献。