Yan Dong

This study shows prenatal e-cigarette exposure causes region- and cell type-specific metabolic and developmental changes in neonatal rat brains, linked to neurodevelopmental disease risk.

This study shows that prenatal THC exposure disrupts mitochondrial gene programs and medium spiny neuron maturation in the nucleus accumbens using snRNA-seq and snATAC-seq in a rat model.

This study shows that astrocytic D1 dopamine receptors in the nucleus accumbens shell regulate synaptic remodeling and cocaine seeking behavior in mice.

The paper examines how NAc neurons shift their activity patterns during cocaine self-administration training, finding expansion and refinement dynamics in neuronal ensembles.

The paper investigates cocaine-induced astrocyte-specific transcriptome in mice, identifies CREB as a key regulator, and shows its role in modulating neuronal and behavioral responses to cocaine.

The paper identifies three temporally sequenced clusters of NAc neuron activity in mice during reward seeking and shows that D1 and D2 neuron activity at specific times predicts and influences lever-pressing behavior.

This study identifies an EEG signature that tracks MCH neuron activity and predicts cocaine seeking behavior in rats.

This study shows that 12/15-Lipoxygenases contribute to neuropathic-like pain hypersensitivity in female mice, with inhibitors reversing pain symptoms.

The paper identifies two BLA subprojections to NAc that differentially encode reward and cue-mediated reinforcement in drug seeking behavior.

The paper characterizes striatal projection neuron heterogeneity in mice using single-nuclei multi-omics and spatial mapping, revealing distinct subtypes with unique receptor expression and disease risk contributions.

The paper identifies FEDORA, a lncRNA with sex- and cell-type-specific effects on depression in females.

The paper identifies protein motifs responsible for enhancing synaptic AMPA receptors through the mutual dependence of Src and PSD-95.

This study shows cocaine induces silent synapse formation via astrocyte-mediated mechanisms, contributing to relapse.

The paper identifies Zfp189 as a key driver of a transcriptional network promoting stress resilience in prefrontal cortex neurons through CREB regulation.