中枢致敏是食管高敏感的重要环节，但目前研究不足。根据食管感觉传入路径及神经纤维解剖投射知识，本研究认为丘脑腹后核是食管高敏感的中枢致敏的关键区域。突触可塑性改变是中枢致敏的重要基础之一，而最近有研究证明ephrin B- Eph B双向信号是调控突触可塑性的关键物质，且涉及到学习、记忆、神经病理性疼痛。则本研究推测ephrin B- Eph B对丘脑腹后核突触可塑性的调控在食管高敏感的发生中起着重要作用。本研究旨在探讨由ehphrinB-EphB双向信号通路调控的丘脑腹后核突触可塑性在食管高敏感发生、发展中的重要作用，明确参与调控丘脑腹后核突触可塑性的Eph B及ephrin B的具体亚型和表达部位、相应的正向和反向通路启动的具体情况、被ehphrinB-EphB调控的具体突触类型（神经元/胶质细胞），了解干预了此信号后食管高敏感的改变情况，从而补充食管高敏感的发病机制。

Central sensitivity which is important to esophageal hypersensitivity is lack of understanding.According to the affernt sensory signal input of the esophagus and the knowledge of neural fiber projection, ventral posterior nucleus of thalamus is thought to be the key brain area related to esophageal hypersensitivity. Synaptic plasticity is one of the most important bases of central sensitivity.Recently, ephrin B- Eph B bidirectional signal was proven as the key substance to control synaptic plasticity and it was thought to be involved in the process of study, memory and neuropathic pain.Hence, we hypothesize that the control of synaptic plasticity by ephrin B- Eph B in ventral posterior nucleus of thalamus is involved in the pathogenesis of esophageal hypersensitivity.We will make sure the exact subtypes and location of ephrin B and Eph B , the activation of the downstream of the bidirectional signal，the exact type of synase (neuron/astrocyte) which was controled, and the change of esophageal sensitivity after blocking or activating the bidirectional signal.The results of this study will be helpful for the understanding of the mechanisms of esophageal hypersensitivity.