COMPARTMENTALIZATION OF ACTION POTENTIAL PROPAGATION IN A POLYAXONAL AMACRINE CELL IN THE MOUSE RETINA

Abstract

Inhibition provided by over 60 types of interneurons called amacrine cells (ACs) diversifies the computational output of the retina. With few exceptions, the specific circuitry and function of individual AC types, however, is poorly understood. Particularly under-studied are so-called wide-field ACs (WACs), neurons with dendrites that can span across millimeters of retina. This expansive coverage is thought to integrate information across broad regions of the visual field and provide postsynaptic partners the ability to respond to spatially modulated stimuli. Retinal ganglion cells (RGCs), the retinal output neurons, are far smaller, and therefore WACs are thought to provide spatial correlation to the responses of RGCs with non-overlapping receptive fields. Prior work from our laboratory identified the nNOS (neuronal nitric oxide synthase)-1 AC as a significant source of inhibitory input and a component of the receptive field surround of the AII AC, an interneuron critical for mediating night vision. Due to this, we believe the nNOS-1 AC acts as a modulator for spatial sensitivity in low light conditions. Interestingly, the nNOS-1 AC has multiple axons that arise from different dendrites and project in various directions. Given that branch points on the neuronal morphology often are considered to be sites at which action potential initiation and propagation can fail, we postulate that nNOS-1 ACs may not provide uniform inhibition to all of their postsynaptic partners and that WAC functionality may be more heterogenous than considered previously. My research utilizes a combination of electrophysiology, functional imaging, and immunohistochemistry to characterize how the nNOS-1 AC generates and propagates signal across its axons. Understanding signal generation in the nNOS-1 AC will provide a deeper understanding of the neural circuitry for night vision and insight into the adaptations that optimize neural structure and physiology to circuit function.