Sensitization of TRPV3 in keratinocytes versus sensory neurons as a mechanism of hyperalgesia

角质形成细胞与感觉神经元中 TRPV3 的敏化作为痛觉过敏的机制

• 批准号: 36145580
• 负责人: Professorin Dr. Katharina Zimmermann
• 金额: --
• 依托单位: Anästhesiologische Klinik
• 依托单位国家: 德国
• 项目类别: Research Fellowships
• 财政年份: 2007
• 资助国家: 德国
• 起止时间: 2006-12-31 至 2007-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/36145580?language=en
• 关键词: Sensitization; TRPV3; keratinocytes; versus; sensory

The contribution of the heat-activated ion channels TRPV3 to the development ofinflammatory and neuropathic hyperalgesia will be investigated using tissue specificconditional knockout mice that lack TRPV3 in keratinocytes and/or DRGs. In vivobehavioural testing and pharmacology and in vitro electrophysiology on nativesensory neurons will be used to find out whether the lack of TRPV3 in eitherkeratinocytes and/or DRGs is responsible for the lack of inflammatory hyperalgesia,i.e. the published phenotype of general TRPV3 deficient mice. Techniques of cellularand molecular biology including also immunohistochemistry and laser TIRF will beused to investigate how sensitization of TRPV3 in either keratinocytes and /or DRGs.The expected findings will provide insight how noxious thermal stimuli are transducedin primary sensory neurons under basal, inflammatory and neuropathic conditions.

将使用角质形成细胞和/或 DRG 中缺乏 TRPV3 的组织特异性条件敲除小鼠来研究热激活离子通道 TRPV3 对炎症和神经性痛觉过敏发展的贡献。对天然感觉神经元的体内行为测试和药理学以及体外电生理学将用于查明角质形成细胞和/或 DRG 中 TRPV3 的缺乏是否导致炎症性痛觉过敏的缺乏，即已发表的一般 TRPV3 缺陷小鼠的表型。细胞和分子生物学技术，包括免疫组织化学和激光 TIRF，将用于研究角质形成细胞和/或 DRG 中 TRPV3 的敏化情况。预期的结果将提供有关在基础、炎症和神经病理条件下有害热刺激如何在初级感觉神经元中转导的见解。