Dear all,

On Friday, April 21 we will welcome for our Bindra lecture Dr. Eric Nestler. Dr. Nestler is a Nash Family Professor of Neuroscience, Director of Friedman Brain Institute, and Dean for Academic and Scientific Affairs at Icahn School of Medicine at Mount Sinai Hospital in NYC.. Dr. Nestler is well-known for his groundbreaking work on the molecular mechanisms of drug addiction and depression. He is a Fellow of the American Academy of Arts & Science and a recipient of numerous awards including the Gold Medal Award from the Society of Biological Psychiatry.

Please put this event (see title and abstract of the talk below) on your calendar and kindly distribute it broadly.

April 21, 3:30

McIntyre Medical Sciences Building, MCMED, 522

Followed by wine and cheese reception on the 8th floor of Stewart Biology.

Dr. Nestler will give a morning lecture in room S2/2 at 10:30-11:30

We hope you can join us all! Karim

Transcriptional and Epigenetic Mechanisms of Depression

Depression is a common, chronic, and debilitating disease. Although many patients benefit from antidepressant medications or other therapies, only about half of depressed patients show a complete remission, which underscores the need for more effective agents. The mechanisms that precipitate depression, such as stress, are incompletely understood. One mystery of the disease is its long-lasting nature and delayed response to antidepressant treatment. This persistence is thought to be mediated by slowly developing but stable adaptations in the brain, which might include regulation of gene expression and chromatin structure. We have used several chronic stress procedures in mice, such as chronic social defeat stress and chronic variable stress, as models of depression that mimic key symptoms seen in humans. An important feature of this work is to examine not only those mice that succumb to the stress (susceptibility), but also those that avoid deleterious outcomes (resilience). We are exploring the molecular basis of stress-induced behavioral pathology, antidepressant action, and resilience by analyzing genome-wide changes in gene expression and chromatin modifications in several limbic brain structures. Parallel work has focused on homologous regions in the brains of depressed humans examined postmortem. We are using these datasets to understand prominent sex differences in stress responses in mice and depression in humans as well as to identify the mechanisms by which early life experience controls stress vulnerability for a lifetime. Together, this work is providing novel insight into the molecular mechanisms underlying depression and other stress-related disorders. The findings also suggest novel leads for the development of new antidepressant treatments. For example, our findings on resilience suggest the novel approach of developing medications that promote resilience and not just those that oppose the deleterious effects of stress.