The widespread misuse of both prescribed and illicit opioids, termed the Opioid Crisis, has grave consequences for both individuals and our society. This project aims to understand the cellular pathophysiology underlying compulsive drug use to enable development of new therapeutic options to treat opioid addiction.
Opioid addiction is a chronic relapsing disease, with most users going through many cycles of use, withdrawal and relapse. Relapse to drug use is promoted by increases in reward seeking during withdrawal (to alleviate the aversive emotional state) and exposure to drug-associated cues. The central idea of this project is that opioids used during opioid withdrawal are more rewarding than under normal conditions. The persistent memory of this elevation of opioid reward value relies on withdrawal-induced synaptic plasticity that persists after the acute withdrawal phase and then drives relapse and promotes compulsive drug use. This project seeks to understand how this withdrawal-induced synaptic plasticity forms as the basis for development of therapies that target the mechanisms responsible for opioid addiction. In particular, this project will focus on the role of endogenous opioids in the amygdala in this process.
Techniques will include patch-clamp electrophysiology, optogenetics, immunohistochemistry and confocal microscopy. All these methods (and many more) are established in the Bagley laboratory.
The opportunity ID for this research opportunity is 2950