Plasticity of Spinal Inhibition in Spinal Cord Injury

脊髓损伤中脊髓抑制的可塑性

• 批准号: 6938536
• 负责人: Kimberly J Dougherty
• 金额: $ 2.47万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-08-09 至 2006-07-08
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6938536
• 关键词: animal tissue; cell population study; electrophysiology; gamma aminobutyrate; gene expression; gene expression profiling; genetic regulation; genetically modified animals; interneurons; laboratory mouse; laser capture microdissection; microarray technology; nervous system regeneration; neural information processing; neural inhibition; neural plasticity; neurochemistry; neurogenetics; neuroregulation; pain; predoctoral investigator; protein structure function; somesthetic sensory cortex; spinal cord injury; voltage gated channel

DESCRIPTION (provided by applicant): GABAergic neurons can be identified in transgenic mice expressing GFP under the control of a GAD67 regulatory element (Oliva et al., 2000). Whole-cell patch recordings permit characterization of the intrinsic membrane properties of visually-identified GABAergic neurons. To study the modifiability of these neurons, their intrinsic and monoaminergic modulatory properties will be characterized in mice with and without chronic spinal transection. Parallel DNA expression profiling of the same population of neurons with LCM will be performed to identify transection-induced alterations in gene expression. Together, these studies will identify and inter-relate physiologic and molecular plasticity in identified GABAergic interneurons. The long-term goal is to identify fundamental molecular and physiological circuits engaged in the control of the spinal inhibitory apparatus. Clinically, identification of the specific monoaminergic receptor subtypes on GABAergic neurons in the spinal cord and the way in which their firing properties are modulated should identify targets for selective control of GABAergic excitability. This can then be manipulated to limit enhanced sensory transmission in lamina I that is thought to occur in various pain states and after SCI.

描述（由申请人提供）：