Abstract
The central amygdala (CeA) is known to be highly involved in mediating itch and anxiety, but the pathways and mechanisms are yet to be fully understood. The goal of this project was to further study two subsets of the neuronal population within the parabrachial nucleus (PBN)-CeA pathway. The first population is itch-responsive PBN neurons, which project to the CeA. These neurons were captured using the targeted recombination in active populations system and were activated using optogenetic stimulation. I found that activating these neurons could cause an increase in spontaneous scratching, but caused no change in pruritogen induced scratching, anxiety-like behaviors, or pain-like behaviors. Additionally, I found that inhibiting these neurons in a chronic itch model could decrease the amount of spontaneous scratching but did not change anxiety-like behaviors. The second population of neurons are CeA neurons that express neuropeptide y receptor 2. When activated with optogenetics, these neurons had a significant decrease in pruritogen induced scratching behaviors, but no change in anxiety-like behaviors or pain-like behaviors. Overall, I found that these two subsets of the neuronal population within the PBN-CeA pathway seem to be itch specific but have opposite effects on itch behavior when activated. Further research is necessary to fully understand how they interact with each other in the itch affective circuit.