我们发现肠神经元突触可塑性改变是PI-IBS持续内脏高敏感形成的重要原因，但突触可塑性改变的关键机制仍不明确。研究表明EphB/EphrinB双向信号在中枢突触可塑性调控中起重要作用，我们首次发现EphB/EphrinB在ENS中表达，且PI-IBS鼠ENS中EphB1、2及EphrinB2表达明显升高。我们推测与中枢神经系统具有类似结构基础的ENS可能存在共同的突触可塑性调控机制，即EphB/EphrinB双向信号参与ENS突触可塑性的变化。因此，EphB/EphrinB是否及如何参与调控ENS突触形态和功能可塑性是本课题的研究重点，我们将通过在体和离体干预EphB/EphrinB及下游关键分子ROCK1、VGLUTs、NMDAR，证实其在PI-IBS ENS突触可塑性调控中的关键点和作用通路，进而明确肠神经元突触可塑性在PI-IBS内脏高敏感形成的机制，为PI-IBS治疗提供可能靶点。

The abnormality of enteric neuronal synaptic plasticity in PI-IBS model mice has been observed in our previous study, which is an important cause of the sustained visceral hypersensitivity in PI-IBS mice, but the key mechanism in regulation of synaptic plasticity is uncertain. Research showed that EphB/EphrinB bidirectional modulating signal plays a critical role in central neuronal synpatic plasticity. We also found EphB/EphrinB existed in ENS, furthermore EphB1,2 and EphrinB2 were over-expressed in the enteric neuron of PI-IBS mice. Therefore, we speculated that there is a common way in the regulation of synaptic plasticity between the ENS and the CNS, while they have the similar structural basis, i.e. EphB/EphrinB signal may participated in synaptic plasticity of ENS. This study will confirm the pivotal role of EphB/EphrinB in the modulation of enteric neuronal synaptic plasticity and in the generation of visceral hypersensitivity in PI-IBS via interfere with the EphB/EphrinB and the key molecular of this pathway in vivo and in vitro respectively. We hope to provide potential new therapeutic target for PI-IBS.