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

Sachs, Benjamin D., et al. “The effects of brain serotonin deficiency on behavioural disinhibition and anxiety-like behaviour following mild early life stress.The International Journal of Neuropsychopharmacology, vol. 16, no. 9, Oct. 2013, pp. 2081–94. Epmc, doi:10.1017/s1461145713000321. Full Text

Wetsel, W. C., et al. Mouse Behavioral Models for Autism Spectrum Disorders. Aug. 2013, pp. 363–78. Scopus, doi:10.1016/B978-0-12-391924-3.00026-0. Full Text

Rodriguiz, Ramona M., et al. “Emergence of anxiety-like behaviours in depressive-like Cpe(fat/fat) mice.The International Journal of Neuropsychopharmacology, vol. 16, no. 7, Aug. 2013, pp. 1623–34. Epmc, doi:10.1017/s1461145713000059. Full Text

Liu, Gumei, et al. “Transient inhibition of TrkB kinase after status epilepticus prevents development of temporal lobe epilepsy.Neuron, vol. 79, no. 1, July 2013, pp. 31–38. Pubmed, doi:10.1016/j.neuron.2013.04.027. Full Text Open Access Copy

Kim, Il Hwan, et al. “Disruption of Arp2/3 results in asymmetric structural plasticity of dendritic spines and progressive synaptic and behavioral abnormalities.J Neurosci, vol. 33, no. 14, Apr. 2013, pp. 6081–92. Pubmed, doi:10.1523/JNEUROSCI.0035-13.2013. Full Text

Besnard, Jérémy, et al. “Automated design of ligands to polypharmacological profiles.Nature, vol. 492, no. 7428, Dec. 2012, pp. 215–20. Pubmed, doi:10.1038/nature11691. Full Text

Por, Elaine D., et al. “β-Arrestin-2 desensitizes the transient receptor potential vanilloid 1 (TRPV1) channel.The Journal of Biological Chemistry, vol. 287, no. 44, Oct. 2012, pp. 37552–63. Epmc, doi:10.1074/jbc.m112.391847. Full Text

Chen, Xin, et al. “Structure-functional selectivity relationship studies of β-arrestin-biased dopamine D₂ receptor agonists.Journal of Medicinal Chemistry, vol. 55, no. 16, Aug. 2012, pp. 7141–53. Epmc, doi:10.1021/jm300603y. Full Text

Lee, Tong H., et al. “Pharmacologically-mediated reactivation and reconsolidation blockade of the psychostimulant-abuse circuit: a novel treatment strategy.Drug Alcohol Depend, vol. 124, no. 1–2, July 2012, pp. 11–18. Pubmed, doi:10.1016/j.drugalcdep.2012.01.021. Full Text