DENTAL SENSORY MECHANISMS

这项研究的长期目标是开发出 预防和治疗牙疼的基础上，更好地了解 导致三叉神经兴奋的膜机制 初级传入神经元的机械刺激。 神经支配牙齿的伤害感受神经元受到热刺激， 机械、渗透和化学刺激。实验证据 与感觉传导的流体动力学理论一致， 牙质。 根据这一理论，外部刺激（无论是热的， 机械的或渗透的）被转化为牙本质中的流体运动 小管，运动变形的感觉神经末梢，并引起兴奋 伤害感受器 流体动力学理论意味着机械敏感的存在 三叉神经末梢中的传感器元件。我们假设 换能器元件是机械敏感离子通道。各种各样的 已知机械敏感性离子通道存在于不同的细胞类型中， 但迄今为止，还没有对三叉神经的这种通道进行研究， 神经元 本研究提案的目标是描述 三叉神经节机械敏感性离子通道的特性 神经元，特别是牙齿传入神经元。 牙痛通常可以追溯到牙髓发炎。以来 已知组织炎症引起伤害感受性神经元的敏化 纤维的机械刺激，这项研究计划的下一个目标是 以确定机械敏感离子的操作特性是否 三叉神经节神经元中的通道被低细胞外 pH或暴露于炎症介质。 这些研究将有助于更好地了解 引起牙痛的感觉/分子事件。

The long term goal of this research is to develop methods for the prevention and treatment of dental pain, based on a better understanding of the membrane mechanisms which lead to the excitation of trigeminal primary afferent neurons by mechanical stimuli. Nociceptive neurons which innervate the teeth are excited by thermal, mechanical, osmotic, and chemical stimuli. Experimental evidence is consistent with the hydrodynamic theory of sensory transduction in the dentine. According to this theory, external stimuli (be they thermal, mechanical,or osmotic) are translated into movements of fluid in dentinal tubules, the movements deform sensory nerve endings and cause excitation of nociceptors. The hydrodynamic theory implies the presence of mechanosensitive transducer elements in trigeminal nerve endings. We hypothesize that the transducer elements are mechanosensitive ion channels. A wide variety of mechanosensitive ion channels are known to exist in different cell types, but thus far there have been no studies on such channels in trigeminal neurons. The goal of this research proposal is to characterize the properties of mechanosensitive ion channels in trigeminal ganglion neurons in general and in tooth afferent neurons in particular. Toothache can often be traced to an inflammation of the tooth pulp. Since tissue inflammation is known to cause the sensitization of nociceptive fibers to mechanical stimuli, the next goal of this research proposal is to determine if the operating characteristics of mechanosensitive ion channels in trigeminal ganglion neurons are altered by low extracellular pH or exposure to inflammatory mediators. Together these studies will contribute to a better understanding of the sensory/molecular events in which cause dental pain.