Inflammatory influence on mechanoreceptor response

炎症对机械感受器反应的影响

• 批准号: 7008598
• 负责人: ROBERT PERRY TUCKETT
• 金额: $ 20.26万
• 依托单位: UNIVERSITY OF UTAH
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-01-15 至 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7008598
• 关键词: C fiber; calcitonin gene related peptide; capsaicin; computer program /software; data collection methodology /evaluation; electrophysiology; histamine; immunocytochemistry; inflammation; laboratory rat; mast cell; mechanoreceptors; neurons; nociceptors; postganglionic fiber; prostaglandin E; serotonin; skin; stimulus /response

DESCRIPTION (provided by applicant): The classic theory of specific nerve energies proposes that sensory information is encoded and transmitted centrally along labeled lines. According to this view, the cutaneous sensory modalities of touch, pain, temperature (warmth, cooling) and itch are encoded by specific classes of peripheral neurons and are transmitted by particular central nervous system pathways. Experimental evidence reveals little overlap of adequate stimuli between axons in different sensory categories. For example, nociceptors fail to respond to low intensity thermal and mechanical stimuli while mechanoreceptors are exquisitely sensitive to stimuli that fail excite nociceptor neurons. On the other hand, there has been little investigation of whether inflammation related changes in skin are able to alter the function of non-nociceptive peripheral neurons. Reaction of the cutaneous slowly adapting type I (SAI) mechanoreceptor to serotonin and other chemical species has long been known, but was thought to be a novelty having little practical significance. However, recent evidence now suggests a complex interaction between mechanoreceptor function and inflammatory processes such as that exposure to capsaicin produces modulation of SAI mechanoreceptor behavior similar to that induced by axon reflex activation. The progressive release of substance P, nitric oxide, and prostaglandin E2 (as well as histamine and serotonin through mast cell degranulation) appears to modulate SAI mechanoreceptor activity at each stage of the inflammatory process. We propose experiments to systematically investigate the influence of neurogenic inflammation on SAI mechanoreceptors and to use irnmunocytochemical techniques to identify the cellular elements within the touch dome that influence the type I/Merkel cell complex.

描述（由申请人提供）：特定神经能量的经典理论提出，感觉信息是沿着标记线集中编码和传输的。根据这一观点，触觉、疼痛、温度（温暖、凉爽）和瘙痒的皮肤感觉形式由特定类别的外周神经元编码，并由特定的中枢神经系统通路传递。实验证据表明，在不同的感觉类别的轴突之间的足够的刺激很少重叠。例如，伤害感受器不能对低强度的热和机械刺激作出反应，而机械感受器对不能激发伤害感受器神经元的刺激非常敏感。另一方面，很少有研究是否炎症相关的皮肤变化能够改变非伤害性外周神经元的功能。 皮肤慢适应I型（SAI）机械感受器对5-羟色胺和其他化学物质的反应早已为人所知，但被认为是一种新奇的，几乎没有实际意义。然而，最近的证据表明机械感受器功能和炎症过程之间存在复杂的相互作用，例如暴露于辣椒素产生SAI机械感受器行为的调制，类似于轴突反射激活诱导的行为。P物质、一氧化氮和前列腺素E2（以及通过肥大细胞脱粒的组胺和5-羟色胺）的逐步释放似乎在炎症过程的每个阶段调节SAI机械受体活性。 我们提出的实验，系统地调查神经源性炎症对SAI机械感受器的影响，并使用免疫细胞化学技术，以确定触摸圆顶内的细胞元素，影响I型/默克尔细胞复合体。