Wang Lab



Celluar and Circuit Neurobiology of Alcohol Use Disorder

Dr. Wang’s research focuses on identifying the neurobiological basis of neuropsychiatric disorders, such as alcohol use disorders. His group investigates the cellular and circuit alterations that occur in areas of the brain in response to excessive, pathological alcohol consumption. They are particularly interested in changes that occur at specific afferent projections onto distinct neuronal populations. They are also interested in contributions of these changes to excessive, pathological alcohol consumption. The results of the research will guide future efforts toward the development of more effective therapeutics for alcohol use disorders.

Dr. Wang participates in graduate training as a member of the faculty in the Interdisciplinary Program in Neuroscience and the Medical Science PhD program in the College of Medicine.


  1. Explore alcohol-mediated input- and cell type-specific plasticity in the striatum
  2. Using a combination of slice electrophysiology, optogenetics, chemogenetics, transgenic animals, and neuropharmacology, Dr. Wang’s group currently investigates alcohol-mediated aberrant plasticity in the dorsal striatum, a major entry structure of the basal ganglia. The dorsal striatum is crucial for habit learning and goal-directed behaviors that are altered in addiction. The dorsal striatum receives a number of different glutamatergic inputs, including corticostriatal and amygdalostriatal afferents, and also contains two groups of principal neurons: dopamine D1 or D2 receptor-expressing medium spiny neurons (D1 or D2 MSNs, respectively). They are interested in elucidating how different afferent glutamatergic inputs in distinct types of neurons within the dorsal striatum are altered by excessive alcohol intake, and how such alterations contribute to excessive alcohol-drinking behaviors.


  3. Ex vivo and in vivo optogenetic reversal of alcohol-mediated circuit-specific plasticity
  4. The few available medications for alcoholisms have limited efficacy and often fail to prevent relapse to alcohol, perhaps because they do not reverse the alcohol-evoked long-term synaptic plasticity, which is believed to drive alcohol seeking and relapse. This project employs dual-channel optogenetics ex vivo and in vivo to reverse alcohol-evoked synaptic plasticity, thereby persistently reducing alcohol seeking and relapse. Long-term potentiation (LTP) and depression (LTD) will be induced identified inputs to striatal D1 or D2 MSNs.