Research

Post-traumatic stress disorder (PTSD), characterized by persistent avoidance of traumatic stress-associated stimuli, is highly co-morbid with alcohol use disorder (AUD). Using lab rats as a model, we have shown that a single episode of bobcat odor exposure produces persistent avoidance of bobcat odor-paired stimuli in a subset of animals (termed Avoider rats), mirroring the individual differences in responsivity to traumatic stress seen in humans. Importantly, Avoider rats go on to show long-lasting increases in alcohol drinking after stress, a phenomenon that is absent in stress-exposed Non-Avoider rats. We are interested in understanding the neurobiology that contributes to these individual/subpopulation differences in stress responsivity, and how they may drive escalation of alcohol drinking after stress. Current work is focused on understanding how various subpopulations of neurons in the hypothalamus respond to traumatic stress, and how their responsivity to alcohol and regulation of alcohol drinking is altered after stress.

In humans, alcohol is well known to alter social behaviors. An area that is understudied is how chronic alcohol misuse contributes to interpersonal problems that stem from increased aggression and violence. In rodents, chronic alcohol drinking increases aggression and violent attacks during aggressive encounters, and heightens the rewarding properties of antagonistic encounters. Current work is focused on elucidating the neural mechanisms that modulate these phenomena, with a special interest on the medial prefrontal cortex and the hypothalamus.