Peter J. Hamilton

This study shows that altering TRIM28 function in the mouse prefrontal cortex leads to transposable element derepression and social behavior deficits, which can be reversed by interferon cytokines.

This study finds that transposable elements are downregulated in the brains of individuals with Major Depressive Disorder, particularly in the orbitofrontal cortex, and this effect varies by age and sex.

This study identifies ZFP189's role in regulating transposable elements in medium spiny neurons, showing how TE activation or repression in specific neuronal subtypes influences cocaine-related behaviors and gene expression.

This study shows that E2F3a overexpression in D1-MSNs increases cocaine reward in both male and female mice, while knockdown has opposite effects, with no impact in D2-MSNs.

The paper identifies sex-specific regulation of stress susceptibility by the astrocytic gene Htra1 in mice and humans, showing differential effects on neuronal signaling and ECM integrity.

The paper investigates whether elevated H1x protein levels in the ventral hippocampus cause stress-related behavioral adaptations, finding no significant behavioral effects from H1x overexpression.

This study identifies transcriptional changes in the brain reward circuit across heroin exposure and seeking behaviors in mice, revealing molecular mechanisms and potential therapeutic targets for opioid use disorder.

This study shows that a synthetic zinc finger transcription factor modulates social behaviors by regulating transposable elements and immune response in the prefrontal cortex of mice.

This study identifies RXR as a key regulator of drug reward sensitivity in the nucleus accumbens through transcriptional control of neuronal excitability in mice.

This study shows that Set2-mediated H3K36me3 regulates alternative splicing of Srsf11, which influences cocaine reward behavior in mice.

This study shows that opioid withdrawal leads to sex-specific changes in fentanyl choice and mesolimbic gene expression in rats, with males showing increased fentanyl preference and females showing transcriptional hyperfunction.

This study shows ketamine restores escape behavior by re-engaging dopamine systems to drive cortical spinogenesis after aversive learning.

The paper analyzes multi-omic data from stressed mice to identify molecular disruptions linked to depression and shows antidepressants reverse these changes in specific brain regions.

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