Nestler Lab

Laboratory of Molecular Psychiatry

Integrating Molecular, Cellular, Systems, and Behavioral Neuroscience

DiverseBrains

Research

The goal of our research is to better understand the molecular mechanisms of addiction and depression. We use animal models of these disorders to identify the ways in which long-term exposure to drugs of abuse or stress changes the brain to lead to addiction- or depression-like syndromes. A major focus of our work is on drug- and stress-induced changes in gene expression and chromatin structure within the brain’s reward circuitry, and the mechanisms by which those lasting adaptations alter neuronal and circuit function to produce behavioral abnormalities.

Nestler Laboratory

Eric Nestler, MD, PhD

Interim Dean, Icahn School of Medicine at Mount Sinai
Executive Vice President & Chief Scientific Officer, Mount Sinai Health System
Nash Family Professor of Neuroscience and Psychiatry

Location
Lab: ICAHN 10-26 | Office: ICAHN 10-23a
Phone
Office: 212.659.5996
Lab: 212.659.5938
Lab fax: 212.659.1559
Admin Fax: 212.659.8510
Email

Publications

Google Scholar

Follow

Grants & Support

National Institute on Drug Abuse

National Institute of Mental Health

Conte Translational Neuroscience Center on Depression

Program Project Grant on the Molecular Neurobiology of Drug Addiction

Hope for Depression Foundation

Featured Publications

Cocaine-context memories are transcriptionally encoded in nucleus accumbens Arc ensembles

Abstract

Learned associations between the rewarding effects of drugs and the context in which they are experienced are critical for context-induced relapse. While context re-exposure triggers the recall of such drug-related associative memories it is unclear whether this relies on the reactivation of and plasticity in neuronal populations previously engaged in their acquisition. Here, using the immediate early gene Arc, we captured a discrete population of nucleus accumbens (NAc) cells activated during the encoding of cocaine-context memory in mice and showed that this neuronal ensemble is later reactivated upon context-induced recall. Furthermore, we show that ensembles recruited at early vs. late stages of memory encoding are largely distinct and contribute differentially to memory retrieval.

Read More

Stress drives myelopoiesis to impair atherosclerosis resolution

Abstract

Atherosclerotic cardiovascular diseases (ASCVD) remain the leading cause of death globally. Animal and human studies link psychological stress-related disorders to ASCVD. Despite this accumulating evidence linking stress to increased cardiovascular disease (CVD) risk, it remains unclear whether stress impairs the benefits of standard risk-reduction therapies, of which lipid-lowering remains the most common, or whether this increased risk is driven by systemic inflammatory states.

Read More

Neurobiology of resilience to early life stress

Abstract

The early years of life are a critical period for brain development, encompassing high sensitivity to adverse experiences. Early life stress (ELS) is known to “scar” the brain and shape mental health trajectories later in life. Still, a great percentage of children faced with ELS develop adaptive competencies that maintain normal physiological and behavioral function across the lifespan, a process referred to as resilience. Work in humans and rodent models has demonstrated that resilience is an active process mediated largely by the induction of unique molecular, cellular, and circuit adaptations.

Read More