THE CIRCUIT COMPONENTS OF CONTRAST ADAPTATION IN THE ROD BIPOLAR PATHWAY
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The mammalian retina processes stimuli over a wide range of light intensities. These stimuli can vary substantially over time. The retina must encode these temporally varying light stimuli into the firing rates of retinal ganglion cells, which convey information from the retina to the brain. This process is called contrast adaptation and relies on circuit-level mechanisms called gain controls. My work seeks to determine which physiological mechanisms within the retina shape the process of adaptation within an inner retinal circuit called the rod bipolar pathway.
This work uses Cre-mediated expression of channelrhodopsin-2 to optogenetically stimulate individual components of the rod bipolar pathway: specifically rod bipolar cells and type-6 cone bipolar cells. This allows for the dissection of mechanisms that shape contrast adaptation within the inner retina, without the significant limitations of paired-patch recording. Much of this work also uses Linear-Nonlinear (L-N) cascade modeling, allowing for the use of naturalistic stimuli to study adaptation.
The first part of this dissertation focuses on several findings that suggest prominent roles for synaptic release from rod bipolar cell terminals, as well as the activity of AII amacrine cells in contrast adaptation within the ON component of the rod bipolar pathway (Chapters 1 & 2). The focus will then switch to experiments examining the OFF component of the rod bipolar pathway (Chapter 3). Finally, this dissertation closes with a series of novel methods developed to address technical challenges that occurred during this work (Chapter 4).