Research in the Mulholland Lab aims to unlock the molecular mechanisms by which chronic alcohol leads to escalation of voluntary consumption and aberrant morphological and synaptic plasticity. We combine various techniques, such as super-resolution confocal imaging and 3D image analysis, electrophysiology, biochemistry, pharmacology, fiber photometry-GCaMP6 signaling, and behavior, to understand the cellular and molecular changes that contribute to alcohol dependence and heavy alcohol drinking.
Dr. Patrick Mulholland is interested in how chronic alcohol exposure produces neuroadaptations in surface trafficking and function of K+ channels that localize to glutamatergic synapses and dendritic membranes. Our previous studies show that alcohol dependence reduces expression of synaptic K+ channels that control glutamatergic signaling, and pharmacologically targeting these channels reduces heavy alcohol drinking. We have also identified strong genetic links between genes encoding select K+ channels and alcohol-related behaviors and phenotypes (i.e., alcohol consumption and alcoholism susceptibility risk). Current efforts in the Mulholland Lab focus on functional and morphological plasticity within the corticoaccumbens circuitry using emerging technologies, and our recent synaptomic studies identified novel alcohol-sensitive proteins and biomarkers across species. These studies aim to define the cellular basis for cognitive dysfunction and relapse to alcohol-seeking behaviors in order to identify novel therapeutic targets to treat alcohol use disorder.