Patrick J. Mulholland

This study examines genetic and physiological changes in the mediodorsal thalamus of alcohol-dependent mice and finds alcohol-biased calcium signaling during choice behaviors.

This study shows that targeting KV7 channels in the prefrontal cortex of alcohol-dependent mice can rescue cognitive deficits and reduce alcohol intake.

The paper shows that alcohol drinking increases calcium activity in mouse central amygdala dynorphin-expressing neurons compared to other solutions.

The paper identifies dysregulated proteins in the orbitofrontal cortex of individuals with alcohol use disorder using proteomics and machine learning, linking them to drinking behavior in mice.

The paper shows that prelimbic cortical neurons encode hedonic value during solution consumption, with distinct activity patterns for water, ethanol, and sucrose, and these patterns are altered by ethanol dependence.

This study identifies sex-specific changes in functional brain connectivity networks in mice with excessive alcohol drinking using whole-brain c-Fos mapping.

This study shows that inhibiting the ventral hippocampus increases ethanol drinking in non-dependent mice but not in dependent mice, suggesting reduced vHC activity contributes to increased drinking.

The paper identifies Kcnn3 as a pharmacogenetic target for reducing ethanol drinking and anxiety-like behaviors in stressed, ethanol-dependent mice.

This study identifies epigenetic changes in KCNN3 gene variants in alcohol-dependent monkeys and mice, linking hypermethylation to altered KCa2 channel function and potential role in alcohol use disorder.

This study uses in vivo fiber photometry to monitor neural activity in mice and rats during exposure to drugs of abuse, revealing changes in calcium transients in brain regions associated with reward and decision-making.