Xueyi Xie

The paper maps input organization of mPFC-projecting basal forebrain cholinergic neurons and identifies weakened striatal-NBM inhibitory transmission in 5xFAD mice.

This paper identifies a CRF pathway in the extended amygdala that enhances striosomal suppression of dopamine during fentanyl withdrawal.

This study shows that extinction training reduces alcohol relapse by suppressing acquisition-recruited striatal ensembles and engaging striosomal neurons in mice.

This paper identifies a CRF-CIN pathway linking the extended amygdala to the dorsal striatum and shows alcohol disrupts CRF-induced cholinergic activity.

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.

This study shows chronic alcohol consumption impairs cognitive flexibility by reducing thalamic excitation of cholinergic neurons in the dorsomedial striatum.