Matthew T. Birnie

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

This study shows that chronic corticosteroid treatment disrupts synaptic structure and cognitive function in the perirhinal cortex.

This study shows chronic corticosteroid exposure disrupts circadian regulation of hippocampal function and synaptic plasticity in rats, leading to memory loss.

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.