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: 31 December 1997

My laboratory uses genetically-modified mice to study the roles that certain genes and gene products play in the expression of abnormal neuroendocrine, neurological, and psychiatric responses. Traditionally, an 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 advent of gene manipulation in mice has permitted specific genes to be targeted for disruption, mutation, and/or overexpression in the whole organism or in selected regions or cells in the nervous and other systems. In this way, primary and secondary effects of a given gene manipulation can be related to various neuroendoctine, neurological, or psychiatric conditions in humans. As the Director of the Mouse Behavioral and Neuroendocrine Analysis Core Facility at Duke University (http://sites.duke.edu/mousebehavioralcore/), we have neurobehaviorally phenotyped many different lines of inbred and mutant mice 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. Following the development of mouse models, we have worked with various investigators to identify the molecular and cellular basis of the neuroendocrine and/or behavioral abnormalities. We are working also with medicinal chemists and certain pharmacological/biotechnological companies to identify novel compounds that will ameliorate abnormal responses in the mutant mice. Some of these preclinical studies are now forming a basis for clinical trials in humans.

Education & Training

  • Ph.D., Massachusetts Institute of Technology 1983

Selected Grants

Cocaine Withdrawal: A Window of Treatment Opportunity awarded by National Institutes of Health (Co Investigator). 1999 to 2010

Collaborative & Physiological Experiments to Breed CPE KO Mice awarded by National Institutes of Health (Principal Investigator). 2006 to 2007

The Pathophysiology of CMT2A in Cell and Animal Models awarded by National Institutes of Health (Co Investigator). 2006 to 2007

Collaborative & Physiological Experiments to Breed CPE KO Mice awarded by National Institutes of Health (Principal Investigator). 2005

Collaborative & Physiological Experiments awarded by National Institutes of Health (Principal Investigator). 2004 to 2005

Genetic Rescue Of Pro-Lhrh Processing In Cpefat Mice awarded by National Institutes of Health (Principal Investigator). 1998 to 2004

Collaborative & Physiological Experiments of CPE K/O Mice awarded by National Institutes of Health (Principal Investigator). 2002 to 2003


Gaier, Eric D., et al. “Peptidylglycine α-amidating monooxygenase heterozygosity alters brain copper handling with region specificity..” J Neurochem, vol. 127, no. 5, Dec. 2013, pp. 605–19. Pubmed, doi:10.1111/jnc.12438. Full Text

Wetsel, William C., et al. “Disruption of the expression of the proprotein convertase PC7 reduces BDNF production and affects learning and memory in mice..” Proc Natl Acad Sci U S A, vol. 110, no. 43, Oct. 2013, pp. 17362–67. Pubmed, doi:10.1073/pnas.1314698110. Full Text

Ruzzo, Elizabeth K., et al. “Deficiency of asparagine synthetase causes congenital microcephaly and a progressive form of encephalopathy..” Neuron, vol. 80, no. 2, Oct. 2013, pp. 429–41. Pubmed, doi:10.1016/j.neuron.2013.08.013. Full Text

Gomes, Ivone, et al. “GPR171 is a hypothalamic G protein-coupled receptor for BigLEN, a neuropeptide involved in feeding..” Proc Natl Acad Sci U S A, vol. 110, no. 40, Oct. 2013, pp. 16211–16. Pubmed, doi:10.1073/pnas.1312938110. Full Text

Sachs, Benjamin D., et al. “The effects of brain serotonin deficiency on behavioural disinhibition and anxiety-like behaviour following mild early life stress..” Int J Neuropsychopharmacol, vol. 16, no. 9, Oct. 2013, pp. 2081–94. Pubmed, 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..” Int J Neuropsychopharmacol, vol. 16, no. 7, Aug. 2013, pp. 1623–34. Pubmed, 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