Using the principles of synaptic plasticity to promote recovery from amblyopia

弱视是一种常见的视力残疾形式，出现在婴儿期和早期 儿童时期，两只眼睛对视觉皮层的输入不平衡（对于 例如，由于眼睛错位、不对称屈光或混浊， 一只眼睛的障碍）。弱视的特征是一只眼睛的视力非常差， 以及随之而来的立体视觉的丧失。对弱视治疗方法的改进的需求是 广泛承认。 过去50年的动物研究揭示了 弱视有充分的文献证明，暂时性单眼剥夺会改变 初级视觉皮层中使皮层神经元无反应的突触强度 对眼睛的刺激。然而，对这些机制知之甚少， 帮助弱视康复我们最近发现， 局部麻醉的视网膜在大脑中产生运动变化， 完全恢复的影响，早期生活单眼剥夺时，麻醉 会慢慢消失我们的目标是揭示这种复苏如何发生的机制， 并确定这些知识是否可以转化为新的和更好的治疗方法， 弱视

Amblyopia is a prevalent form of visual disability that arises during infancy and early childhood when inputs to the visual cortex from the two eyes are poorly balanced (for example, by misalignment of the eyes, asymmetric refraction, or opacities and obstructions of one eye). Characteristics of amblyopia are very poor acuity in one eye, and an attendant loss of stereopsis. The need for improved treatments for amblyopia is widely acknowledged. Animal studies over the past 50 years have uncovered the pathophysiology of amblyopia. It is well documented that temporary monocular deprivation alters the strength of synapses in primary visual cortex that renders cortical neurons unresponsive to stimulation of the deprived eye. However, much less is known about the mechanisms that serve recovery from amblyopia. We recently discovered that temporarily inactivating the retinas with a local anesthetic sets in motion changes in the brain that enable complete recovery from the effect of early life monocular deprivation when the anesthetic wears off. Our objectives are to uncover the mechanism for how this recovery occurs, and to determine if this knowledge can be translated into new and better treatments for amblyopia.