Patricia Janak

Patricia Janak is the Bloomberg Distinguished Professor at Johns Hopkins University, holding dual affiliations in the Department of Psychological and Brain Sciences (Krieger School of Arts & Sciences) and the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins School of Medicine. Her research focuses on understanding the neural and behavioral mechanisms of associative learning and their role in addiction. She utilizes animal models, optogenetics, and in vivo electrophysiology to study how brain regions like the amygdala, nucleus accumbens, and dopamine pathways regulate reward-seeking and maladaptive behaviors.

Patricia Janak earned her PhD from the University of California, Berkeley. Her work bridges basic neuroscience with translational research, aiming to uncover how environmental cues and neural circuits contribute to relapse in alcohol and drug addiction. Key projects include investigating dopamine’s role in reward prediction, the amygdala’s encoding of cue-outcome associations, and the impact of chronic ethanol exposure on cognitive flexibility.

Her research interests emphasize the interplay between brain circuits and behavioral control, particularly in contexts involving reward, fear, and decision-making. Recent studies explore sex-dependent differences in addiction, the neural basis of habitual behaviors, and how optogenetic tools can disrupt alcohol-seeking behaviors. Awards and grants are not explicitly listed, but her lab’s extensive publications reflect significant contributions to addiction neuroscience.

Patricia Janak advises and mentors lab members through her roles in both departments, focusing on training in advanced neurobiological techniques. The Janak Lab collaborates across disciplines to map neural circuits involved in addiction, with a current emphasis on the nucleus accumbens, basolateral amygdala, and mesolimbic dopamine systems. Her work also examines therapeutic interventions, such as mTORC1 inhibition and pharmacological modulation of GABAA receptors, to disrupt relapse mechanisms.