Synaptic and intrinsic mechanisms underlying visual cortical enhancement following retinal inactivation

项目摘要 弱视是人类视力残疾的一种普遍形式，是由于视觉质量的差异造成的 眼睛在出生后的早期。这种差异促使视觉皮层中的眼优势可塑性倾向于 以较弱的眼睛（弱视）为代价的较强的眼睛。因此，视觉皮层中的突触 弱视眼的下游被削弱，这是一个很难逆转的过程，除非治疗， 在婴儿期或幼儿期开始。最近在动物模型中的研究提出了几种策略， 促进弱视的康复。虽然弱视的病理生理学已经得到了很好的研究， 恢复背后的突触和细胞条件不太清楚。这项提案的重点是一种治疗方法， 通过暂时性失活细胞因子快速促进实验性弱视后视力恢复的策略 视网膜暂时的视网膜失活导致视觉皮层的稳定增强 一旦视力恢复。这项提案的目的是确定视网膜失活如何改变 突触，细胞和电路水平的属性，以促进视觉皮层的增强。长期目标 这项研究的目的是了解皮质可塑性如何促进恢复，并为临床提供信息。 用于治疗人类弱视的干预。

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.