Giulia Zanni, BSC, MSC, PhD

I am a translational neuroscientist interested in how the circuits, cells, and synapses of the developing brain are influenced by experience. My career research goal is to pinpoint which and how anatomical, molecular, and neural circuit mechanisms acting in development contribute to pathological motivated behaviors. At each step, I have maintained a clinically translational and a developmental neurobehavioral focus to my research. My expertise is on modeling complex human behavior using rats or mice that recapitulates human behavior.
My work has focused on the brain's regenerative capacity and how brain plasticity can be harnessed to restore maladaptive cognitive and emotional outcomes arising from early life insults. From my PhD thesis, I first authored several publications on lithium 's restorative effects of neurogenesis, particularly improving cognition after irradiation of the developing brain. The results from my thesis are the basis of an ongoing clinical trial (https://clinicaltrials.gov/study/NCT06051240).
My subsequent first authored publications, in addition to my lithium work, range from developmental models of anxiety and aggression to endophenotypes and sex differences in a paradigm of voluntary access to oxycodone and the repercussions of maternal opioid use on the neonatal opioid withdrawal syndrome, a major public health concern in the United States.
At present, I am a NIMH K01 awardee at Columbia University/RFMH mentored by Drs. Mark Ansorge, Kevin Bath, Jay Gingrich, and Regina Sullivan focused on the role of early life perturbations of serotonin (5-HT) circuits modulating fear. Developmental alterations of monoamine signaling, induced by environmental exposure to drugs, autism, and early life adversities, may represent key mechanistic drivers of depressive-like symptoms such as anxiety, anhedonia, and helplessness. I want to pinpoint which anatomical, molecular, and neural circuit mechanisms acting in development contribute to these pathological behaviors. I use early-life increases in 5-HT and DA signaling as a mechanistically grounded developmental model of psychiatric disorders, with a specific focus on threat responses and reduced motivation behavioral states. This approach reframes psychopathologies not as disorders that emerge de novo in adulthood, but as the long-term behavioral manifestation of developmentally maladapted neural circuits. By modeling psychopathology such as anxiety, depression, and PTSD at their developmental origin rather than at their symptomatic endpoint, this work aims to identify causal circuit mechanisms that underlie emotional and motivational deficits and to reveal earlier, more effective windows for intervention in developmentally rooted neuropsychiatric disorders.
To address these questions, I employ circuit-specific viral strategies, projection-specific manipulations, in vivo fiber photometry and electrophysiology, and automated, high-resolution behavioral analyses that capture the temporal structure of defensive and motivated behaviors.
The significance of this approach is to understand the root causes of mood-related psychiatric disorders, rather than focusing on symptom-centric adult models, and to find therapeutic targets that can prevent the emergence of or define the early targets for psychiatric disorders.