William Christopher Wetsel

William Christopher Wetsel

Associate Professor in Psychiatry and Behavioral Sciences

External Address: 
354 Sands Bldg, Durham, NC 27710
Internal Office Address: 
Box 103203 Med Ctr, Durham, NC 27710


Last Updated: 27 October 2020

My laboratory uses genetically-modified mice to study the roles that certain genes and gene products play in the presentation of abnormal neuroendocrine, neurological, and psychiatric responses. Traditionally, the identification of neuroendocrine dysfunction has involved biochemical analyses of hormonal responses, those for neurological disorders have relied upon behavioral and postmortem analyses, and those for psychiatric conditions have depended upon phenomenology.  The use of genetic technologies has allowed specific genes in selected cells and in neural pathways to be related to certain molecular, biochemical, cellular, physiological, and behavioral dysfunctions. As the Director of the Mouse Behavioral and Neuroendocrine Analysis Core Facility at Duke University (http://sites.duke.edu/mousebehavioralcore/), we have phenotyped many different lines of inbred and mutant mice for my own work as well as for investigators at Duke and at other research institutions. As a consequence, we have helped to develop many different mouse genetic models of neuroendocrine and neuropsychiatric illness. We are working also with academic medicinal chemists and/or certain pharmacological/biotechnological companies to identify novel compounds that will ameliorate abnormal responses in various mutant mouse models. Some of these preclinical studies have formed a basis for clinical trials in humans.

Education & Training

  • Ph.D., Massachusetts Institute of Technology 1983

Selected Grants

Amphetamine-Induced Transcriptional Plasticity in Striatal GABAergic Interneurons awarded by National Institutes of Health (Co Investigator). 2012 to 2015

Prevention of Temporal Lobe Epilepsy awarded by National Institutes of Health (Collaborator). 2012 to 2014

Regulation of response to chronic antidepressant treatment by MeCP2 awarded by National Institutes of Health (Co Investigator). 2012 to 2014

Imaging NFkB Activity in Relation to Animal Behavior in Peripheral Neuropathy awarded by National Institutes of Health (Collaborator). 2013 to 2014

Novel Genetic Mouse Model to Study the Consequences of TorsinA Dysfunction awarded by National Institutes of Health (Co Investigator). 2011 to 2014

Non-invasive Chemical Genetic Control of Neuronal Activity awarded by National Institutes of Health (Collaborator). 2009 to 2014

Agilent Direct Drive 9.4T MRS/MRI Console awarded by National Institutes of Health (Major User). 2012 to 2013

PTSD-like phenotype of mice lacking GIT2 awarded by National Institutes of Health (Investigator). 2010 to 2012

Hormonal regulation of a Ca2+/AMPK signaling pathway awarded by National Institutes of Health (Collaborator). 1984 to 2011

Epigenetic regulation of transcriptional repression by drugs of abuse awarded by National Institutes of Health (Co Investigator). 2006 to 2011


Park, Su M., et al. “Effects of β-Arrestin-Biased Dopamine D2 Receptor Ligands on Schizophrenia-Like Behavior in Hypoglutamatergic Mice.Neuropsychopharmacology, vol. 41, no. 3, Feb. 2016, pp. 704–15. Pubmed, doi:10.1038/npp.2015.196. Full Text

Cheng, Jianjun, et al. “Further Advances in Optimizing (2-Phenylcyclopropyl)methylamines as Novel Serotonin 2C Agonists: Effects on Hyperlocomotion, Prepulse Inhibition, and Cognition Models.J Med Chem, vol. 59, no. 2, Jan. 2016, pp. 578–91. Pubmed, doi:10.1021/acs.jmedchem.5b01153. Full Text

Farrell, Martilias S., et al. “In Vitro and In Vivo Characterization of the Alkaloid Nuciferine.Plos One, vol. 11, no. 3, 2016, p. e0150602. Pubmed, doi:10.1371/journal.pone.0150602. Full Text

Nagy, Eniko, et al. “Reproduction and Growth in a Murine Model of Early Life-Onset Inflammatory Bowel Disease.Plos One, vol. 11, no. 4, 2016, p. e0152764. Pubmed, doi:10.1371/journal.pone.0152764. Full Text Open Access Copy

Wu, Chia-Lung, et al. “Dietary fatty acid content regulates wound repair and the pathogenesis of osteoarthritis following joint injury.Ann Rheum Dis, vol. 74, no. 11, Nov. 2015, pp. 2076–83. Pubmed, doi:10.1136/annrheumdis-2014-205601. Full Text

Scott, John W., et al. “Autophosphorylation of CaMKK2 generates autonomous activity that is disrupted by a T85S mutation linked to anxiety and bipolar disorder.Sci Rep, vol. 5, Sept. 2015, p. 14436. Pubmed, doi:10.1038/srep14436. Full Text

Cheng, Y., et al. “Neurotrophic factor-α1 prevents stress-induced depression through enhancement of neurogenesis and is activated by rosiglitazone.Molecular Psychiatry, vol. 20, no. 6, June 2015, pp. 744–54. Epmc, doi:10.1038/mp.2014.136. Full Text

Kim, Il Hwan, et al. “Spine pruning drives antipsychotic-sensitive locomotion via circuit control of striatal dopamine.Nature Neuroscience, vol. 18, no. 6, June 2015, pp. 883–91. Epmc, doi:10.1038/nn.4015. Full Text

Sachs, Benjamin D., et al. “Serotonin deficiency alters susceptibility to the long-term consequences of adverse early life experience.Psychoneuroendocrinology, vol. 53, Mar. 2015, pp. 69–81. Epmc, doi:10.1016/j.psyneuen.2014.12.019. Full Text

Cheng, Jianjun, et al. “Optimization of 2-phenylcyclopropylmethylamines as selective serotonin 2C receptor agonists and their evaluation as potential antipsychotic agents.J Med Chem, vol. 58, no. 4, Feb. 2015, pp. 1992–2002. Pubmed, doi:10.1021/jm5019274. Full Text