DirectVote Election: Candidate Bios Councilor Slot 2 Your Voting Status: Select 0 to 1 from below. Selected: 0 Vote For: Lisa Monteggia Lisa Monteggia Administrative Accomplishments: I have been involved in numerous administrative roles at UT Southwestern Medical Center, including Faculty Search Committees, membership in the Animal Resource Center advisory committee, Institutional Animal Care and Use Committee, Graduate Student Admissions committee, as well as the development of the Behavioral Core Facility. These opportunities have provided me with the skills and experience to deal with the needs and operations of basic science —in particular animal research— in a complex medical school campus. Degree, Institute, Year Earned: BS, University of Illinois-Urbana, 1989 MS, University of Illinois-Urbana, 1991 PhD, The Chicago Medical School, 1998 Postdoctoral fellow, Yale University, 1998-2000 Research Areas: My research interest is the molecular and cellular mechanisms underlying psychiatric disorders and neuropsychiatric treatment strategies. My laboratory studies two critical areas of translational brain research, mechanisms underlying antidepressant action and synaptic alterations that lead to the pathophysiology of the Rett syndrome. Our focus is on the role of synaptic plasticity mechanisms that may underlie these disorders and suggest potential targets for therapeutics. Current Position(s) at Your Current Institution: Ginny and John Eulich Professorship in Autism Spectrum Disorders, Professor of Neuroscience, UT Southwestern Medical Center Memberships: Society for Neuroscience Government and Public Affairs Committee, 2016-present Program Committee, 2013-2016 Professional Development Committee, 2009-2012 https://www.directvote.net/sfn/app/bio_page.aspx?item=4&option=4001&return=ballot_page.aspx[5/11/2017 3:10:50 PM] DirectVote Election: Candidate Bios American College of Neuropsychopharmcology Fellow Membership Committee, 2016-present Strategic Planning Task Force, 2015 Honorific Awards Committee, 2014 Membership Advisory Task Force, Chair, 2014 The Serotonin Club Member Service Positions: A. Editorial Boards: eLife Board of Reviewing Editors, 2017-present Neuropharmacology Editorial Board, 2017-present Behavioral Neuroscience Consulting Editorial Board, 2014-present Journal of Neuroscience Editorial Board, 2013-present Journal of Biological Chemistry Editorial Board, 2013-present Neuropsychopharmacology Reviewing Editor, 2010-present Biological Psychiatry Editorial Board, 2010-present B. Other Service Positions: NIMH Board of Scientific Counselors Ad hoc review member, 2016 Molecular and Cellular Cognition Society (MCCS) Council Member, 2015-present International Rett Syndrome Foundation Scientific Review Board, 2009-present National Institute of Mental Health Pathway to Independence Award (K99/R00) review panel, 2009-present National Institute of Health Study Section Member (MNPS), 2009-2013 Science Biography: I started my career working in drug discovery for a pharmaceutical company focused on developing treatments for neurological disorders. This experience provided a broad perspective on various aspects of neuroscience towards understanding complex brain disorders. As a graduate student in Dr. Marina Wolf’s laboratory, at Chicago Medical School, I began investigating the role of neuronal plasticity in drug addiction. I joined Dr. Eric Nestler’s laboratory, at Yale University, and studied the role of neurotrophic factors in adult brain with an emphasis on synaptic plasticity mechanisms. As an independent investigator, I have continued to study plasticity mechanisms underlying two areas of research, antidepressant efficacy and Rett syndrome. Our first important finding in the field of antidepressant efficacy was that the growth factor, brain- derived neurotrophic factor (BDNF), is required to mediate an antidepressant effect in preclinical animal models. We extended this finding to show that BDNF, specifically in the hippocampus, is necessary for antidepressant action through presumed effects on synaptic plasticity mechanisms. We also showed that gender differences observed in depressed humans, with females being more vulnerable, can be recapitulated in this BDNF mouse model. More recently, we have been investigating the cellular mechanisms that underlie the ability of ketamine, a compound with NMDA receptor antagonist properties, to produce rapidly acting antidepressant responses. We found that NMDA receptor blockade at rest de-suppresses protein translation and potentiates excitatory https://www.directvote.net/sfn/app/bio_page.aspx?item=4&option=4001&return=ballot_page.aspx[5/11/2017 3:10:50 PM] DirectVote Election: Candidate Bios synapses, thereby triggering rapid behavioral antidepressant responses. These and other results suggest a synaptic basis for the antidepressant effects of ketamine. We have also recently shown that the ketamine metabolite, 2R,6R-HNK, blocks synaptic NMDA receptors and recruits the same signal transduction pathway as ketamine in mediating a rapid antidepressant response. These studies indicate the importance of NMDA receptors, coupled to intracellular signaling, in ketamine- mediated rapid antidepressant effects and provide a framework for points of convergence in understanding antidepressant efficacy. Our work may contribute towards the development of more effective treatments for depression. In a second line of research, we have been studying the role of MeCP2, the gene linked to Rett Syndrome, at the behavioral as well as synaptic levels. Although loss of function mutations of MeCP2 cause Rett syndrome, the mechanisms by which such mutations lead to abnormalities in behavior, as well as the underlying functional mechanisms, have remained unknown. We have shown that mice with altered MeCP2 expression selectively in the forebrain exhibit a range of behavioral abnormalities reminiscent of symptoms seen in humans with Rett syndrome. This loss of MeCP2 function results in dramatic alterations in basal excitatory neurotransmission in hippocampus, which is mediated by presynaptic mechanisms and appears to be due to MeCP2’s role as a transcriptional repressor. MeCP2 is an epigenetic factor that is linked to changes in DNA methylation and histone deacetylase (HDAC) activity. We have extended our work to investigate the role of other epigenetic factors, specifically DNA methyltransferases and individual HDACs, in synaptic transmission and complex behavior. This work delineates how epigenetic mechanisms may regulate properties of neurotransmission in the CNS and may point to strategies for novel treatments. Curriculum vitae (pdf opens in a new window) 2 https://www.directvote.net/sfn/app/bio_page.aspx?item=4&option=4001&return=ballot_page.aspx[5/11/2017 3:10:50 PM].