Howard C. Becker

This study identifies PSTN Crh neurons as a key driver of alcohol drinking escalation in dependence, showing their role shifts from inhibitory to stimulatory with dependence.

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 tirzepatide reduces alcohol consumption and relapse-like behaviors in rodents by affecting reward systems and metabolic parameters.

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

The paper uses c-fos mapping and network analysis to show that alcohol dependence alters brain network activity during abstinence and reaccess in mice, with increased network modularity in high-drinking mice after reaccess.

This study identifies transcriptomic changes in the nucleus of the solitary tract (NTS) in response to alcohol dependence and stress, highlighting IFN signaling and specific genes linked to increased alcohol consumption.

The paper identifies brain regional gene expression networks affected by chronic ethanol exposure and consumption in mice, finding unique patterns in prefrontal cortex and nucleus accumbens.

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 shows that CRF-R1 regulates VTA-GABAergic plasticity, which is suppressed by CB1 receptor inhibition after chronic alcohol exposure.