When going from a dark movie theater into the bright sunshine, vision is initially overwhelmed by the suddenly bright light levels, but after time we are again able to see well. This process, called light adaptation, involves a change in the sensitivity of neurons in the retina of the eye. Although retinal adaptation to brighter light levels is a crucial function of the visual system, the changes that happen in the retina to enable this adaptation are not well understood. Previous work has suggested that release of the chemical dopamine from retinal neurons is responsible for light adaptation, but the details of how this works are not clear. This study will determine what changes are occurring in the retina to allow adaptation to increasing light levels and determine how dopamine is changing visual signaling. Additionally, since the retina is an easily accessible part of the brain, these experiments can be used as a model for how dopamine changes the responses of groups of neurons. Dopamine signaling is important throughout the brain and in disorders such as Parkinson's disease. As part of this research, educational materials will also be developed with students to explain how light adaptation works and the importance of this process for normal vision. These materials will be used to increase interest in science for high school students, many of whom are underrepresented in science, and the public through outreach at a yearly festival and web interactions.
Light adaptation is a crucial retinal signaling mechanism that allows the visual system to avoid saturation by resetting the gain of neuronal signaling. Light adaptation also increases visual acuity by increasing the response of ganglion cells, the output neurons of the retina, to small light stimuli. Inhibition of bipolar cells, which relay information to ganglion cells, influences ganglion cell spatial resolution. Therefore, light adaptation modulation of bipolar cell inhibition could increase visual acuity. However, the role of inhibition in light adaptation is not known. Modulation of inhibition may be especially important to adaptation of the retinal pathway that responds to the offset of light (OFF), as inhibitory inputs to OFF-bipolar cells switch between dim light rod and bright light cone sources and light adaptation decreases the spatial extent of inhibition to OFF-bipolar cells. This suggests a model where light adaptation narrowing of bipolar cell inhibition underlies the changes in ganglion cell spatial signaling. It is unknown how narrowing of OFF-bipolar cell inhibition will affect OFF-ganglion cell signaling or what mechanisms underlie the OFF-bipolar cell changes. Dopamine is a key neuromodulator of retinal light adaptation. Dopamine-mediated uncoupling of gap junctions and/or increases in inhibitory connections between upstream neurons might narrow OFF-bipolar cell inhibition. However, the role of dopamine modulation of physiological inhibition is not known. These proposed mechanisms for light adaptation of OFF pathway inhibition and their effects on retinal acuity will be tested using a combination of single-cell electrophysiology, morphology, genetic mouse models and optogenetic activation of retinal neurons.
