CONTRIBUTIONS OF GENETICALLY DEFINED INTERNEURON SUBTYPES TO CONTRAST CODING IN MOUSE PRIMARY VISUAL CORTEX
In the past decade the mouse primary visual cortex (V1) has become a popular brain region for investigating how neural circuits process information, largely because of the genetic tools available in this animal model. One of the most revolutionary genetic tools developed has been optogenetics, which refers to genetically-inserted light-sensitive proteins that are targeted to specific cell types. The ability to selectively activate individual cell types in specific brain regions provides scientists with a level of temporal and spatial resolution not previously available. This thesis contains two projects that take advantage of optogenetics to study an inhibitory circuit involved in visual processing in mouse V1. This inhibitory circuit is primarily composed of three interneuron (IN) subtypes: parvalbumin-expressing (PV+), somatostatin-expressing (Sst+) and vasoactive intestinal peptide -expressing (VIP+) INs. We individually activated these IN subtypes to investigate how they contribute to contrast coding. The first project examined how INs affect Pyramidal (Pyr) cell responses to varying levels of contrast, and our findings suggest that IN functionality is dependent on the state of the Pyr cell’s local network. The second study examined whether individually activating INs affects how Pyr cells adapt to contrast, and our findings indicate that adaptation magnitude depends more on the overall activity level of V1 than which IN subtype is activated, although VIP+ INs appear to have a novel modulatory role. Overall, the findings from this thesis suggest that INs dynamically modulate contrast responses in mouse V1 as opposed to each subtype having an individual role as was previously thought.