Current advisor: Rotating in the lab of Harrison W. Gabel, PhD
Undergraduate university: Duke University
The goal of this research project is to understand how cellular history or context can impact how it responds to neuromodulators. This phenomenon may be able to explain why different pharmacological agents used to treat neuropsychiatric disorders may have a different impact on everyone.
I hoped to elucidate the molecular mechanisms by which one cell can receive the same stimulus and yet produce a different response (as measured by an increase or decrease of PKA activation). We hypothesize this is based on the history/priming from a cell’s previous activity/context. Specifically, I will be observing how the PKA activity of cells within the striatum respond to priming via stimulation of D1 receptors via dopamine. This priming is subsequently followed by stimulation of muscarinic receptors via acetylcholine. Our hypothesis is that dopamine (a neuromodulator important for several behavioral contexts such as reward learning) primes neuronal cells in the striatum by increasing PKA activity within the cells, which can modulates how cells respond to future activation.