Circuit specializations of developing visual networks

项目总结/摘要 胎儿大脑的视觉通路在出生前是高度活跃的。在缺乏高质量视觉线索的情况下， 胎儿视网膜中的自发和光诱发活动提供了主要的视觉输入， 新生啮齿动物在正常的视觉发育和视觉通路的组织中涉及这种早期活动。 虽然我们对在胎儿视网膜中产生活动的专门回路了解很多， 由于大脑活动中断对眼睛和大脑的影响，我们对实际的大脑活动知之甚少。 支持完整动物视觉发育的最早阶段。我们最近的实验表明， 早期视网膜活动不是被动地传递到视觉皮层。相反，它被积极地放大， 由发育中的大脑所特有的机制转化。该提案将使用啮齿动物模型的胎儿 大脑发育，以跟踪早期视网膜活动在每个阶段的传播和转化， 丘脑和视皮层的初级视觉通路，并探讨其转化机制。这 知识是至关重要的，因为与早产或缺氧性出生相关的早期视网膜活动中断 并发症可导致持久的视力损害。任何治疗或早期诊断（如使用EEG） 将需要正常的发展活动模式的知识，这一项目将提供。

Project Summary/Abstract The visual pathways of the fetal brain are highly active before birth. In the absence of high quality visual cues, spontaneous and light-evoked activity in the fetal retina provide the primary visual input, and data from neonatal rodents implicate this early activity in normal visual development and organization of visual pathways. While we understand much about the specialized circuits that produce activity in the fetal retina, and the consequences of disruption of that activity for eye and brain outcomes, we know little of the actual brain activity that supports the earliest stages of visual development in the intact animal. Our recent experiments show that early retinal activity is not passively transmitted to the visual cortex. Rather, it is actively amplified and transformed by mechanisms unique to the developing brain. This proposal will use a rodent model of fetal brain development to follow the propagation and transformation of early retinal activity at each stage of the primary visual pathway in thalamus and visual cortex, and identify the mechanisms of its transformation. This knowledge is critical because disruption of early retinal activity associated with preterm birth or hypoxic birth complications can cause lasting visual impairment. Any treatment or early diagnosis (such as using EEG) would require knowledge of the normal developmental activity patterns, which this project will provide.