Inflammatory influence on mechanoreceptor response

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）和瘙痒的皮肤感觉模式由特定类别的外周神经元编码，并通过特定的中枢神经系统途径传递。实验证据表明，不同感觉类别的轴突之间很少有足够的刺激重叠。例如，伤害感受器不能对低强度的热刺激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，关于皮肤炎症相关变化是否能够改变非伤害性外周神经元功能的研究很少。

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.