DENTAL SENSORY MECHANISMS

这项研究的长期目标是为 在更好的理解基础上，预防和治疗牙痛 导致三叉神经兴奋的膜机制 机械刺激的初级传入神经元。 支配牙齿的伤害性神经元受到温度的刺激， 机械的、渗透的和化学的刺激。实验证据是 与感觉神经传导的流体力学理论一致 牙本质。根据这一理论，外部刺激(无论是热刺激， 机械的，或渗透的)被转化为牙本质中的液体运动 小管，运动使感觉神经末梢变形并引起兴奋 伤害性感受器。 流体力学理论暗示了机械敏感性的存在。 三叉神经末梢中的转导元件。我们假设 换能器元件是机械敏感离子通道。种类繁多的 已知机械敏感离子通道存在于不同类型的细胞中， 但到目前为止，还没有关于三叉神经这种经络的研究。 神经元。这项研究提案的目标是描述 三叉神经节机械敏感离子通道的特性 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。自.以来 已知组织炎症可引起伤害性感受器的敏化 纤维到机械刺激，这项研究提案的下一个目标是 确定机械敏感离子的工作特性 细胞外低氧改变三叉神经节神经元的通道 PH值或接触炎症介质。 这些研究将有助于更好地理解 导致牙齿疼痛的感觉/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.