Lisa M. Monteggia, Ph.D.
Professor of Pharmacology
Barlow Family Director of the Vanderbilt Brain Institute
- : firstname.lastname@example.org
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7140 Medical Research Building III
465 21st Avenue South
Nashville, Tennessee - 37240-7933
- : Lisa M. Monteggia, Ph.D. - CV
Dr. Lisa Monteggia is the Barlow Family Director of the Vanderbilt Brain Institute and Professor of Pharmacology at Vanderbilt University. Dr. Monteggia completed her undergraduate studies at the University of Illinois at Urbana-Champaign, receiving a B.S. in Microbiology and then a M.S. in Biology. Dr. Monteggia then worked for several years in a pharmaceutical company where she was promoted to the level of Scientist. Concurrently, Dr. Monteggia attended the Chicago Medical School receiving a Ph.D. in Neuroscience and working with Dr. Marina Wolf in the area of drug abuse. Dr. Monteggia then moved to Yale University to complete a fellowship under the guidance of Dr. Eric Nestler in the area of molecular psychiatry. Dr. Monteggia joined the faculty at UT Southwestern Medical Center where she held the Ginny and John Eulich Professorship in Autism Spectrum Disorders and was Professor of Neuroscience at UT Southwestern Medical Center before moving to Vanderbilt in 2018.
The main focus of the Monteggia laboratory is on the molecular and cellular mechanisms that underlie psychiatric disorders. Our work to date covers two critical areas of molecular neuroscience. First, we have been investigating the role of neurotrophins, in particular brain-derived neurotrophic factor (BDNF), and the TrkB receptor in adult brain function using conditional and inducible cell type specific knockout mice. Our early work established a critical role for BDNF in determining antidepressant efficacy as well as certain aspects of depressive like behavior. More recently, we have been investigating the mechanism underlying the rapid antidepressant action of ketamine. Our second area of research aims to elucidate the role of MeCP2, a transcription factor, in synaptic function and behavior using mouse models of Rett syndrome. Our work has identified key synaptic deficiencies associated with Rett syndrome and defined specific brain regions that give rise to symptoms associated with the disorder in mouse models. Furthermore, this work also led to an investigation of epigenetic factors, including MeCP2 and HDACs, that regulate synapse maturation and synaptic efficacy in the central nervous system. Epigenetic regulation of synapse function carries wide ranging implications that go beyond the etiology of Rett syndrome to mechanisms underlying other disorders including traumatic brain injury. Within the laboratory we combine advanced molecular, cellular, behavioral, and electrophysiological studies to probe these critical scientific questions at multiple steps, and thereby establish causal links among these diverse levels of analysis. These multi-based approaches are critical for understanding the brain, and yield insight into the study of depression, Rett syndrome, as well as related brain disorders.
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