Circuit specializations of developing visual networks

项目摘要/摘要 胎儿大脑的视觉通路在出生前非常活跃。在没有高质量视觉提示的情况下， 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，数据来自 新生啮齿动物的这种早期活动与正常的视觉发育和视觉通路的组织有关。 虽然我们对在胎儿视网膜中产生活动的特殊回路了解很多，但 这种活动中断对眼睛和大脑结果的影响，我们对实际的大脑活动知之甚少 这支持了完好动物视觉发育的最早阶段。我们最近的实验表明， 早期的视网膜活动并不是被动地传递到视皮层。相反，它被积极放大和 由发育中的大脑所特有的机制转变。这项提议将使用啮齿动物模型的胎儿 大脑发育跟踪早期视网膜活动在每个阶段的传播和转换 丘脑和视皮层的初级视觉通路，并确定其转化机制。这 知识至关重要，因为早期视网膜活动中断与早产或缺氧性出生有关 并发症可能会导致永久性的视力损害。任何治疗或早期诊断(例如使用脑电波) 需要了解正常的发展活动模式，这是这个项目将提供的。

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.