Identification of CaMKII as a novel substrate of dopaminylation following heroin self administration

Substance Use Disorders arise from a complex interaction of synaptic and epigenetic plasticity, whereby modulation of dopaminergic signaling result in long lasting aberrant plasticities and harmful behavioral outcomes. This project examines a novel mechanism for synapse-to-nucleus dopaminergic signaling, one which would likely illuminate a new conceptual understanding of how dopamine functions in the brain, and have possibly broad implications outside the field of substance abuse research. The studies proposed here hold the potential to explain unanswered questions in dopamine-mediated pathophysiology of substance use disorders, as well as novel therapeutic targets therein.