The visual pathways of the human fetal brain are highly active before birth. During this pre-visual period spontaneous activity in the retina provides the primary input to visual brain and data from neonatal rodents implicate this early activity in normal development and organization of visual pathways. While we understand much about the specialized circuits that produce activity in the developing retina, and the consequences of disruption of that activity for eye and brain outcomes, we know little of the brain activity that supports the earliest stages of sensory development. Early retinal activity is not passively transmitted in the developing brain. Rather, it is actively amplified and transformed by mechanisms unique to this developmental stage. This proposal will use a rodent model of human 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, to understand the mechanisms of its transformation, the role of individual thalamic regions, and the ultimate impact of this circuit on functional visual maps and responsiveness. This knowledge is important because disruption of early retinal, thalamic, or cortical activity associated with preterm birth or hypoxic birth complications can cause lasting visual impairment. Any treatment or early diagnosis (such as using EEG) requires knowledge of the normal developmental circuitry, activity and function of thalamus and cortex, which this project will provide.