DISTRIBUTION AND ULTRASTRUCTURE OF DENTAL INNERVATION

牙齿神经支配的分布和超微结构

基本信息

批准号：
6286951
负责人：
MARGARET READ BYERS
金额：
$ 35.21万
依托单位：
UNIVERSITY OF WASHINGTON
依托单位国家：
美国
项目类别：
财政年份：
1979
资助国家：
美国
起止时间：
1979-05-01 至 2004-01-31
项目状态：
已结题

项目摘要

Dental innervation is still not fully understood concerning its variety of nerve fibers, their interactions with pulp and dentin in normal teeth, and the mechanisms that cause hypersensitive dentin, postoperative pain, and difficult anesthesia for inflamed teeth. There is important plasticity in expression of sodium channels in injured cutaneous sensory neurons, driven by neurotrophic factors, but it is not known whether similar events underlie persistent neuroplasticity and pain after tooth injury. Teeth are an excellent model tissue for studying neuroinflammatory interactions in the periphery and their effects on trigeminal nerves, the ganglion and the central nervous. Tooth injury also affects non-dental neurons in the ganglion, in the brain stem and sometimes in contralateral trigeminal neurons by mechanisms that in part depend on paracrine signalling by nerve growth factor. The Aims of this work are: (1) to determine the effects of specific types of tooth injury on sodium channel expression in dental neurons, neighboring uninjured trigeminal neurons and central neurons in relation to pain behavior, pulpal pathology and anti-inflammatory treatment, (2) to determine whether trigeminal sodium channel expression, pulpal reactions and behavior are affected in mutant mice that have altered neurotrophin mechanisms, and (3) to define the complexities of cells in the pulp, especially the odontoblast layer, in relation to expression of neurotrophins and calcium channels, in order to better understand the pulpal-nerve interactions in normal and injured teeth. We will use dental injury models in rats and mutant mice for analysis by behavioral testing, immunocytochemistry and in situ hybridization. There will be specific labeling of injured dental neurons by retrograde transport of fluorogold for comparison with uninjured labeled neurons. Our newly developed behavioral assays allow the characterization of pain periods in relation to pulpal and neural cytochemistry during anti-inflammatory treatment or in mutant mice. Our goal is to understand neuroinflammatory interactions in inflamed teeth in order to develop better treatments for dental pain.

关于其神经纤维的多样性，与正常牙齿中的牙髓和牙本质的相互作用以及引起过度敏感性牙本质的机制，术后疼痛以及发炎牙齿的困难麻醉的机制，牙齿神经支配仍然尚未完全理解。由神经营养因素驱动的受伤皮肤感觉神经元中钠通道的表达有重要的可塑性，但尚不清楚牙齿损伤后持续性神经可塑性和疼痛是否是基于类似的事件。牙齿是一种出色的模型组织，用于研究周围神经炎性相互作用及其对三叉神经，神经节和中枢神经的影响。牙齿损伤还会影响神经节中的非牙科神经元，在脑干中以及对侧三叉神经元中的非牙科神经元，这部分依赖于神经生长因子的旁分泌信号传导。这项工作的目的是：（1）确定特定类型的牙齿损伤对牙齿神经元中钠通道表达的影响，相对于疼痛行为，性性病理学和抗炎治疗的邻近的未受伤的三叉神经元和中心神经元与中心神经元相关（2）（2）（2），以确定三方通道表达的反应性，是促成腐蚀性的反应机制。（3）与神经营养蛋白和钙通道的表达相关的纸浆中细胞的复杂性，尤其是Odontoblast层的复杂性，以便更好地理解正常牙齿和受伤的牙齿中的牙髓神经相互作用。我们将使用大鼠和突变小鼠中的牙科损伤模型通过行为测试，免疫细胞化学和原位杂交分析。通过氟胶质的逆行运输，将与未受伤的标记神经元进行比较，将受伤的牙齿神经元进行特定的标记。我们新开发的行为分析允许在抗炎治疗期间或突变小鼠中与牙髓和神经细胞化学有关的疼痛时期的表征。我们的目标是了解发炎牙齿中的神经炎性相互作用，以开发更好的牙齿疼痛治疗方法。