Optogenetic Interrogation of Primary Visual Cortex and Its Impact On Neural Coding and Behavior

<p>Understanding the mechanism by which the brain transforms simple sensory inputs into rich perceptual experiences is one of the great mysteries of systems neuroscience. Undoubtedly this involves the activity of large populations of interconnected neurons, but while the responses of individual neurons to a variety of sensory stimuli have been well-characterized, how <em>populations</em> of such neurons organize their activity to create our sensory perceptions is almost entirely unknown. To investigate this complex circuitry requires the ability to causally manipulate the activity of neural populations and monitor the resultant effects. Here we focus on primary visual cortex (V1), which has been shown to be crucial for visual perception, and utilize optogenetic tools to render the activity of genetically- defined neural populations sensitive to light. By simultaneously recording and modulating (either driving or silencing) the activity of excitatory (glutamatergic) neurons, we are able to causally examine their role in visual perception. Here we report 3 major findings. First, we show that activating subpopulations of excitatory neurons can improve visual perception under certain conditions and that information in V1 used for perceptual decisions is integrated across spatially-limited populations of neurons. Further, we show that a key signature of this information integration is a reduction in correlated variability between neurons. Correlated variability has been implicated as a major source of behavioral choice related activity in the cortex, and theorized to be a major factor limiting information in cortical populations. However, until now, there has not been a way to manipulate correlations without altering firing rates or other task related variables. Here we demonstrate a novel method using optogenetic stimulation to causally manipulate correlated variability between cortical neurons without altering their firing rates. Lastly, with the goal of expanding the currently limited repertoire of optogenetic tools for non-human primates, we establish the viability of a novel optogenetic construct capable of dramatically silencing neural populations using a recently discovered anion conducting channelrhodopsin.</p>

Name thesis:degree_name

Doctor of Philosophy (PhD)

Level thesis:degree_level

Dissertation (PhD)

Year dc:date.available

2017

Authors dc:creator

• Andrei, Ariana R
• <p>0000-0003-2152-2580</p>

Contributors dc:contributor

• Roger Janz, PhD
• John H. Byrne, PhD
• Daniel J. Felleman, PhD

• Primary visual cortex
• V1
• macaca mulatta
• electrophysiology
• optogenetics
• channelrhodopsin
• behavior
• detection
• Behavioral Neurobiology
• Systems Neuroscience

Repository record dc:identifier

https://digitalcommons.library.tmc.edu/utgsbs_dissertations/747

OAI identifier oai:identifier

oai:digitalcommons.library.tmc.edu:utgsbs_dissertations-1837