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弱视是一种儿童早期由于异常的视觉经历如斜视，屈光参差，视觉剥夺等导致的皮层性视觉损害，因而，只有理解了其发病的神经机制，才可能提出有效的治疗。一般观念认为弱视只有在儿童期治疗才有效，而成人的弱视基本无法治愈，但是近年来随着对弱视发病机制的分子生物学及神经电生理的研究，尤其是对视觉皮层发育可塑性的细胞间交流及细胞内分子信号通路的认识，拓展了人们对弱视病理的知识，因而也成功地通过恢复成年期的可塑性改善了成年弱视的视力。本文介绍了视觉发育可塑性的进展，就近年在增强成年可塑性途径如改变神经兴奋性与抑制性的平衡、细胞外基质、丰富环境及表观遗传学修饰等作了介绍，以其对弱视的病理机制，尤其对成人弱视的治疗有更深入的认识。“,”Amblyopia is a form of cerebral visual impairment caused by abnormal visual experience ( e.g., strabismus, anisometropia, deprivation) during early childhood. It is essential to understand the neural mechanism of amblyopia in order to devise novel therapeutic strategies. Although previous concepts of amblyopia is an untreatable pathology in adults, recent data deepen our knowledge of the factors involved in the intercellular communication and intracellular signaling that mediate experience-dependent plasticity in the developing visual cortex. Successful en-hancement of adult plasticity has been achieved by altering the excitation to inhibition balance;extracellular matrices;environmental enrichment and epigenetic modification. In this review, I describe current concepts of brain plasticity and the established mechanisms of amblyopia, and their implications for novel therapeutic strategies, these may hold the best hope for success in the fight against amblyopia.