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Elizabeth Lucas, Ph.D.

Assistant Professor, Neurobiology

Office: 919.513.1885
Lab: Lucas Lab
Lab Phone: 919.513.1885
Lab Fax: 919.513.7301

Dr. Lucas joined the Department of Molecular Biomedical Sciences as an Assistant Professor in January 2018. Dr. Lucas’s doctoral and postdoctoral training has spanned almost every subdiscipline of neuroscience, from molecular to systems to behavioral. Her doctoral research was conducted in the laboratory of Dr. Rita Cowell in the Department of Psychiatry and Behavioral Neurobiology at the University of Alabama at Birmingham (UAB). She combined molecular biology with genetic approaches in mouse models to determine novel region- and cell-specific gene targets of a transcriptional coactivator implicated in neurodegenerative and neuropsychiatric illness. Her thesis was highlighted by the remarkable discovery that the transcriptional coactivator acts as a master regulator of gene programs necessary for the maturation and maintenance of cortical interneurons. Following her successful PhD work, Dr. Lucas the lab of Dr. Roger Clem as a postdoctoral fellow in the Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai in New York City. There she incorporated optogenetic approaches with in vitro slice electrophysiology to examine experience-dependent plasticity of neural circuits after emotional learning. She found that emotional memory encoding results in persistent downregulation of inhibition in the amygdala, the emotional processing center of the brain, through extensive plasticity of local inhibitory interneurons. In addition to her research accomplishments, Dr. Lucas also has taught graduate- and undergraduate-level courses in statistics and molecular genetics at UAB and New York University. Dr. Lucas particularly enjoys mentoring students toward the completion of honors and thesis projects, and she and her students have received numerous accolades for their research. Her research program at NC State will utilize novel techniques, including cell-specific optogenetics, chemogenetics, and neural ensemble tagging, to elucidate novel cells and circuits underlying fear-, anxiety-, and depression-related behavior in mouse models.
Society for Neuroscience
W.M. Keck Center for Behavioral Biology
New York Academy of Sciences
Graduate Women in Science
B.S. in Psychology, University of Alabama at Birmingham (2005)
Ph.D. in Behavioral Neuroscience, University of Alabama at Birmingham (2011)
Postdoctoral Fellow, Icahn School of Medicine at Mount Sinai (2017)
Research in the Lucas Lab is driven by a passion to improve the lives of people with mental illness. We conduct preclinical research in animal models to understand the mechanisms underlying susceptibility to psychiatric illness, with an emphasis on sex as a biological factor. Women are twice as likely as men to be diagnosed with fear-, anxiety-, and mood-based psychiatric disorders, but the exclusion of female subjects in preclinical research has hindered our progress in elucidating the sex-specific neurobiological bases of such illnesses. Our laboratory utilizes a multifaceted, systems-based approach that combines in vivo behavioral manipulations with ex vivo electrophysiological, transcriptional, anatomical, and endocrinological analyses in mouse models to dissect the neurobiological mechanisms underlying sex differences in behavioral states relevant to mental illness at the levels of the cell and the circuit. This research seeks to expand upon previous research conducted by ourselves and others, in hopes of attaining novel, potentially sex-specific, therapeutic targets for devastating mental illnesses disproportionally experienced by women, for which there are currently limited effective treatments and no cures.
  • (2017) GABAergic interneurons: the orchestra or the conductor in fear learning and memory? In pressLucas, E.K. & Clem, R.L. | Brain Research Bulletin.
  • (2016) Multimodal and site-specific plasticity of amygdala parvalbumin interneurons after fear learning.Lucas, E.K., Jegarl, A.M., Morishita, H., & Clem, R.L. | Neuron, 91, 3: 629-643.
  • (2016) Cortical PGC-1α-dependent transcripts are reduced in postmortem tissue from patients with schizophrenia.McMeekin, L.J., Lucas, E.K., Meador-Woodruff, J.H., McCullumsmith, R.E., Hendrickson, R.C., Gamble, K.L., & Cowell, R.M. | Schizophrenia Bulletin, 42, 4: 1009-1017.
  • (2015) Interneuron transcriptional dysregulation causes frequency-dependent alterations in the balance of inhibition and excitation in hippocampus.Bartley, A.F., Lucas, E.K., Brady, L.J., Li, Q., Hablitz, J.J., Cowell, R.M., & Dobrunz, L.E. | Journal of Neuroscience, 35, 46: 15276-15290.
  • (2015) Cerebellar transcriptional alterations with Purkinje cell dysfunction and loss in mice lacking PGC-1α.Lucas, E.K., Reid, C.S., McMeekin, L.J., Dougherty, S.E., & Cowell, R.M. | Frontiers in Cellular Neuroscience, Special Issue, Neurodegeneration: from Genetics to Molecules, 8, 441: 1-13.
  • (2014) PGC-1α provides a transcriptional framework for synchronous neurotransmitter release from parvalbumin-positive interneurons.Lucas, E.K., Dougherty, S.E., McMeekin, L.J., Reid, C.S., West, A.B., Dobrunz, L.E., Hablitz, J.J., & Cowell, R.M. | Journal of Neuroscience, 34, 43: 14375-14387.
  • (2014) Mice lacking TrkB in parvalbumin-positive cells exhibit sexually dimorphic behavioral phenotypes.Lucas, E.K., Jegarl, A., & Clem, R.L. | Behavioural Brain Research, 274: 219-225.
  • (2014) Mice lacking the transcriptional coactivator PGC-1α exhibit alterations in inhibitory synaptic transmission in the motor cortex.Dougherty, S.E., Bartley, A.F., Lucas, E.K., Dobrunz, L.E., Hablitz, J.J., & Cowell, R.M. | Neuroscience, 271: 137-148.
  • (2013) Abnormal expression of glutamate transporters in temporal lobe areas in elderly patients with schizophrenia.Shan, D., Lucas, E.K., Drummond, J.B., Haroutunian, V., Meador-Woodruff, J.H., & McCullumsmith, R.E. | Schizophrenia Research, 144 (1-3): 1-8.
  • (2012) Developmental alterations in motor coordination and medium spiny neuron markers in mice lacking PGC-1α.Lucas, E.K., Dougherty, S.E., Trinh, A.T., Reid, C.S., McMeekin, L.J., & Cowell, R.M. | PLoS ONE, 7, 8: e42878.
  • (2012) Disruption of Purkinje cell function prior to huntingtin accumulation and cell loss in an animal model of Huntington Disease.Dougherty, S.E., Reeves, J. L., Lucas, E. K., Gamble, K. L., Lesort, M., & Cowell, R.M.  | Experimental Neurology, 236: 171-178.
  • (2010) Neuronal inactivation of PPARγ coactivator 1α (PGC-1α) protects mice from diet-induced obesity and leads to degenerative lesions.Ma, D., Li, S., Lucas, E.K., Cowell, R.M., & Lin, J.D. | Journal of Biological Chemistry, 285, 10: 39087-39095.
  • (2010) Parvalbumin deficiency and GABAergic dysfunction in mice lacking PGC-1α.Lucas, E.K., Markwardt, S.J., Gupta, S., Meador-Woodruff, J.H., Lin, J.D., Overstreet-Wadiche, L., & Cowell, R.M. | Journal of Neuroscience, 30, 21: 7227-7235.
  • (2009) Do perceptually salient stimuli reduce children’s risky decisions?Schwebel, D.C., Lucas, E.K., & Pearson, A. | Journal of Clinical Psychology in Medical Settings, 16, 3: 223-232.
  • (2007) Unintentional injury risk in children with externalizing behavior disorders at summer camp.Schwebel, D. C., Tavares, C. L., Lucas, E. K., Bowling, E. B., & Hodgens, J. B. | Journal of Clinical Psychology in Medical Settings 14, 2: 145-151