Eric J. Nestler

Biosketch

Eric Nestler is the Nash Family Professor of Neuroscience and Psychiatry and Interim Dean at the Icahn School of Medicine at Mount Sinai. He earned his MD (1983) and PhD (neuropharmacology, 1982) from Yale University and completed residency training in psychiatry also at Yale in 1987. He then joined the Yale faculty where he rose through the ranks to become the Jameson Professor of Psychiatry and Neurobiology and Founding Director of the Division of Molecular Psychiatry. In 2000, he was named the McGinley Distinguished Professor and Chair of Psychiatry at UT Southwestern at Dallas, before moving to Mount Sinai in 2008 as Chair of the Department of Neuroscience and Founding Director of the Friedman Brain Institute. He was named Dean for Academic and Scientific Affairs in 2016, became Chief Scientific Officer in 2021, and was appointed interim Dean in 2025. Nestler served as President of the American College of Neuropsychopharmacology in 2011 and as President of the Society for Neuroscience in 2017. He is a member of the National Academy of Sciences, National Academy of Medicine, and American Academy of Arts and Sciences. He is the recipient of the Peter Seeburg Integrative Neuroscience Prize (Society for Neuroscience), Redelsheimer Distinguished Award (Society of Biological Psychiatry), Wilbur Cross Distinguished Alumnus Medal (Yale University), Sarnat Prize in Mental Health (National Academy of Medicine), and Patricia Goldman-Rakic Award (Brain and Behavior Research Foundation). He has honorary doctorate degrees from Uppsala University and Concordia University.

Research Interests

My laboratory focuses on understanding the molecular, cellular, and circuit changes that mediate the brain’s long-lasting adaptations to environmental experience. Most of the laboratory’s work is performed within the context of drug addiction or depression, studying how chronic exposure to drugs of abuse or to stress induces addiction- or depression-related outcomes in rodent models. Human postmortem brain tissue from individuals with these disorders is examined in parallel to ensure a focus on clinically-relevant mechanisms. Indeed, we have shown that certain rodent models recapitulate large swaths of the molecular pathology seen in homologous brain regions of the human syndromes. Animal models are required to ascertain whether a change seen in humans is maladaptive (pathogenic) or adaptive (pro-resilient), to elaborate the underlying mechanisms, and to leverage the advances for eventual clinical translation. The laboratory’s work concentrates on drug- or stress-induced, cell-type-specific changes in gene expression within key limbic brain regions and the detailed transcriptional and chromatin mechanisms that mediate these changes. We then establish causal links between a molecular change and altered functioning of the affected cell type, and altered functioning of the larger circuit in which that cell type operates, to ultimately mediate behavioral change. In the course of this work, my laboratory played a key role in pioneering several novel experimental approaches including viral-mediated gene transfer and locus-specific neuroepigenomic editing in vivo.