运动融合中枢异常可塑性在间歇性外斜视发病中作用及其Synapsin调控机制

斜视是影响儿童眼健康的最主要眼部疾病之一，既往研究认为双眼运动融合储备力降低与间歇性外斜视发病有关，但无法解释患者随病程延长运动融合储备力变化规律及其对斜视的影响机制。我们研究发现，双眼运动融合需要运动融合中枢(FEF)调控；突触蛋白(Synapsin)水平对小鼠初级视觉中枢发育可塑性起重要作用，但在运动融合中枢可塑性及斜视中作用尚待研究。据此，我们提出Synapsin参与运动融合中枢可塑性调控并导致间歇性外斜视发病的假说。本研究拟构建间歇性外斜视猫模型，明确猫运动融合中枢可塑性关键期；利用慢病毒过表达Synapsin，阐明关键期内异常视觉经验通过Synapsin影响运动融合中枢可塑性的机制；运用功能磁共振联合运动融合功能检查，探讨间歇性外斜视患者运动融合中枢功能变化，揭示运功融合中枢异常可塑性与间歇性外斜视发病之间的关系。所获成果有助于发现间歇性外斜视的关键致病因素，为其防治提供新思路。

Strabismus is one of the most important ocular diseases in children. Previous studies have suggested that the decrease of binocular fusional reserves be related to the onset of intermittent exotropia (IXT). However, it cannot explain the patterns of fusion reserves in the progress of IXT or how it works on strabismus. Our studies have found that binocular fusional vergence is regulated by fusional vergence center (frontal eye fields, FEF). We have also found that the level of synapsin may play an important role in mouse primary visual center plasticity, but its role in fusional vergence plasticity and strabismus remains to be clarified. Based on the above studies, we propose that synapsin be involved in the regulation of fusional vergence center plasticity and result in the onset of IXT. We intend to explore the critical period of fusional vergence center plasticity by using the cat model with IXT. Furthermore, the molecular mechanism of synapsin in fusional vergence center plasticity in critical period will be investigated by lentivirus transfection. At the same time, to reveal the role of aberrant fusional vergence center plasticity in the pathogenesis of IXT, the fusional vergence center function in IXT patients will be detected by functional magnetic resonance imaging (fMRI) and fusional vergence examinations. The achievements of this study will help discover the essential pathogenesis of IXT and provide new ideas for its prevention and treatment.