注视性眼球运动失稳在异常视觉经验导致视皮层神经回路重塑中的作用与机制研究

弱视是视觉发育期内由于异常视觉经验引起的单眼或双眼最佳矫正视力下降，其患病率高达3%。探索弱视发病机制具有指导临床诊治和认识大脑机制的双重意义。既往观点认为弱视的视功能损害主要是由于视觉感觉通路（主要是视中枢）发生了经验依赖的神经联系的可塑性修饰与重塑，而眼球运动系统在弱视发生机制中的作用长期被忽视。近年来的一系列研究进展提示，注视性眼球运动在视觉信息的处理中起着极其重要的作用。我们最新的研究结果也证实，弱视患者弱视眼的注视性扫视运动存在着明显的异常，相关的数学模型推测，注视性扫视运动可影响外侧膝状体-视皮层的神经联系，并调控视皮层神经元的反应特性。为此，本课题拟采用棉耳绒猴为对象，利用高速视频眼动记录、细胞外记录、在体膜片钳全细胞记录、视觉诱发电位、行为学、神经药理等多种技术手段，探讨注视性眼球运动在视觉发育关键期内异常视觉经验引起的视皮层神经回路重塑中的作用及其神经生物学机制。

Amblyopia refers to reduced best corrected vision in one or both eyes caused by abnormal visual experience during visual development period, which morbidity is up to 3%. To explore the mechanism of amblyopia has double significance for both guiding clinical diagnosis and therapy for amblyopia and understanding the brain mechanism. The traditional opinion is that the visual functional impairment in amblyopia is mainly due to the experience dependent plastic modification and reconstruction of neural circuitry along the sensory visual pathway (mainly visual cortex), while the effect of ocular motility on the pathogenesis of amblyopia has long been neglected. A series of research advances in the recent years suggested that the fixational eye movements play a significant role in the visual processing. Our latest research results confirmed that the amblyopes' amblyopic eyes showed significant abnormality of their fixational saccadic eye movements. Other researchers' mathematical model further suggest that fixational saccadic eye movements can affect the neural connections form lateral geniculate nucleus to visual cortex and also modulate the response characteristics of visual cortical neurons. Therefore, this study will use the cotton-eared marmosets as research animals, and apply multi technical means of high speed video based eye tracker,extracellular recording, in vivo patch clamp whole-cell recording, visuial evoked potentials recording，behavior test，and neuropharmacology, etc., to explore the effect of fixational eye movements on the remodeling of visual cortical neural circuitry caused by abnormal visual experience during the critical period of visual development and its neurobiological mechanism.