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.
The fetal retina produces activity that guides normal development of the visual system. This project will explore how the fetal brain actively amplifies and transforms this input into a form uniquely suited for early visual maturation, using a rodent model of fetal brain development. Our long term objective is to understand the special role that fetal rhythms play in the maturation of vision, to be able to identify and treat consequences of preterm birth and perinatal brain injury such as cerebral visual impairment.
