Synaptic and intrinsic mechanisms underlying visual cortical enhancement following retinal inactivation

项目摘要 弱视是人类普遍存在的一种视觉障碍，由两者之间的视觉质量差异引起 出生后早期的眼睛。这种差异驱使视觉皮质中的眼优势可塑性倾向于 以弱视(弱视)为代价的强眼。因此，视觉皮质中的突触 弱视眼的下游会变弱，这一过程很难逆转，除非进行治疗 在婴儿期或幼年早期开始的。最近在动物模型中的研究已经提出了几种策略 促进弱视的康复。虽然弱视背后的病理生理学已经得到了很好的研究， 康复背后的突触和细胞条件还不太清楚。这项提议的重点是一种治疗 通过暂时灭活弱视促进实验性弱视后视力恢复的策略 视网膜。视网膜暂时失活期导致视觉皮质的稳定增强 一旦视力恢复，就会有反应。这项提议的目标是确定视网膜失活是如何改变的 突触、细胞和电路水平的特性，以促进视觉皮质增强。长期目标 这项研究的重点是了解皮质可塑性是如何促进恢复的，并为临床提供信息 治疗人类弱视的干预措施。

Project Summary Amblyopia is widespread form of human visual disability caused by a disparity in visual quality between the two eyes during early postnatal life. This disparity drives ocular dominance plasticity in the visual cortex to favor the stronger eye at the expense of the weaker (amblyopic) eye. Consequently, synapses in the visual cortex downstream of the amblyopic eye are weakened, a process that is difficult to reverse unless treatment is initiated during infancy or early childhood. Recent work in animal models has suggested several strategies for promoting recovery from amblyopia. While the pathophysiology underlying amblyopia has been well studied, the synaptic and cellular conditions underlying recovery are less clear. This proposal focuses on a treatment strategy that rapidly promotes visual recovery following experimental amblyopia via temporary inactivation of the retinas. A temporary period of retinal inactivation leads of a stable enhancement of visual cortical responses once vision is restored. The goal of this proposal is to identify how retinal inactivation alters synaptic, cellular, and circuit-level properties to promote visual cortical enhancement. The long-term objective of this research is to understand how cortical plasticity is engaged to promote recovery and to inform clinical interventions for treating human amblyopia.