Vision requires the precise organization and function of neuronal circuits in the retina. Our overall goal here is to advance the basic understanding of the cellular mechanisms that regulate the formation and the maintenance of synaptic connections in the mammalian retina. Like elsewhere in the nervous system, signals not only converge onto individual neurons from multiple input types, but signals from an individual neuron are also distributed across multiple targets. Together, these two basic motifs of synaptic connectivity, convergence and divergence, underlie the complex but highly organized processing of neuronal information. Our knowledge of the mechanisms that sculpt stereotypic patterns of convergence is expanding. In contrast, our understanding of how divergence is shaped during development and disrupted in neurodegenerative conditions is scarce. To fill this gap in knowledge, we will focus on the AII amacrine cell circuitry that is integral to the rod pathway, which is responsible for scotopic vision. This circuit will enable us to gain insight into the developmental mechanisms that organize an exquisite arrangement of synaptic divergence at a single synapse (Aim 1), as well as mechanisms that distribute synapses from a single cell in a biased but consistent manner across distinct targets (Aim 2). We will use a combination of novel imaging approaches, electrophysiology and transgenic animals to: (Aim 1) Determine the cellular mechanisms that organize synaptic divergence at the rod bipolar cell - AII/A17 amacrine cell dyad, and ascertain the factors that lead to disruption of this synapse after neurodegeneration due to a rise in intraocular pressure (IOP), and: (Aim 2) Determine the cellular processes that shape output connections of AII amacrine cells onto bipolar cells and ganglion cells during normal development, and identify the processes that disrupt these connections upon IOP elevation. Together, our findings will greatly advance knowledge of the mechanisms responsible for precision in circuit assembly, as well as offer new knowledge of how this precision becomes altered in conditions of neuronal degeneration.