Xuehua Wang

This study shows that alcohol and opioids modulate glutamatergic input to the SCN, revealing the SCN as a target of depressant substances and highlighting glutamatergic transmission as a vulnerability in circadian dysregulation.

This study shows that abstinence and extinction training lead to opposing changes in striatal activity and dopamine signaling during alcohol relapse, with extinction reducing relapse-like behavior.

This study shows that traumatic brain injury increases alcohol consumption and impairs cognition by reducing cholinergic activity and increasing microglial cells in mice.

This study examines how chronic alcohol exposure affects corticostriatal circuits and pathology in two Alzheimer's disease mouse models, revealing distinct effects on Aβ and tau-driven pathologies.

This study shows that prenatal alcohol exposure reduces cholinergic interneurons and their activity in the striatum, leading to impaired cognitive flexibility and compulsive drinking behaviors in adult offspring.

The paper inhibits striatal engrams involved in alcohol-taking behaviors to show reduced future alcohol-seeking and enhanced extinction.

This study shows that burst firing of striatal cholinergic interneurons promotes extinction learning, while their pause is critical for reversing goal-directed behavior, and alcohol disrupts this process.

This paper shows that drug reinforcement impairs cognitive flexibility by inhibiting striatal cholinergic interneurons through enhanced inhibitory transmission from direct-pathway medium spiny neurons.

This study shows that chronic opioid use induces GABAergic plasticity in striatal neurons, leading to hypodopaminergic states and negative affect, which contribute to relapse.