Yuncai Chen

The paper identifies sex-dependent roles of paraventricular thalamus neurons in mediating the effects of early-life adversity on adult reward behaviors in mice.

The paper identifies disrupted CRH signaling as a cause of reward deficits after early-life stress and shows CRHR2 activation can reverse anhedonia-like behaviors.

The paper investigates how early-life adversity affects reward behaviors through peptide signaling in the paraventricular thalamus and identifies CRHR1 as a molecular target for intervention.

The paper investigates sex differences in memory vulnerability to acute traumatic stress, finding that estrogen and its receptors play a role in both males and females.

The paper investigates sex- and stress-dependent plasticity of a CRH/GABA projection from the BLA to NAc, showing differential effects on reward behaviors in males and females.

The paper validates a novel Crhr1-FlpO mouse that selectively targets CRHR1-expressing neurons for genetic manipulation.

The paper identifies a novel stress-sensitive CRH GABA projection from the basolateral amygdala to the nucleus accumbens that contributes to reward behavior disruption following early-life adversity.

The paper identifies the thalamic paraventricular nucleus (PVT) as a region selectively activated by early-life adversity (ELA) in mice, linking it to long-term reward-related behavioral deficits.

This study uses single-cell RNA sequencing to identify lasting transcriptional changes in hypothalamic CRH-expressing neurons after early-life adversity, linking these changes to long-term stress responses.