Using the principles of synaptic plasticity to promote recovery from amblyopia

弱视是一种常见的视力残疾，出现在婴儿期和早期。 儿童时期，从双眼到视觉皮质的输入不平衡(对于 例如，由于眼睛不对准、不对称屈光或不透明 一只眼的阻塞)。弱视的特点是一只眼的视力非常差， 以及随之而来的立体视觉的丧失。弱视治疗方法的改进是有必要的 广为人知。 在过去的50年里，动物研究揭示了 弱视。有充分的证据表明，暂时性的单眼剥夺会改变 初级视皮层突触强度使皮质神经元无反应 刺激被剥夺的眼睛。然而，人们对这种机制知之甚少。 为弱视的康复服务。我们最近发现，暂时失活 含有局部麻醉剂的视网膜启动了大脑的变化，使 完全恢复早期生活单眼剥夺时的麻醉效果 会慢慢消失的。我们的目标是揭示这种复苏如何发生的机制， 并确定这种知识是否可以转化为新的更好的治疗方法 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.