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
Phone: 
919.684.4574

Overview

RESEARCH INTERESTS
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

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

Stress and Behavior in Health and Disease awarded by National Institutes of Health (Mentor). 1989 to 2011

Pages

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.Mol Psychiatry, vol. 20, no. 6, June 2015, pp. 744–54. Pubmed, 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.Nat Neurosci, vol. 18, no. 6, June 2015, pp. 883–91. Pubmed, 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. Pubmed, 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

Weitzel, Douglas H., et al. “Radioprotection of the brain white matter by Mn(III) n-Butoxyethylpyridylporphyrin-based superoxide dismutase mimic MnTnBuOE-2-PyP5+.Mol Cancer Ther, vol. 14, no. 1, Jan. 2015, pp. 70–79. Pubmed, doi:10.1158/1535-7163.MCT-14-0343. Full Text

Hunanyan, Arsen S., et al. “Knock-in mouse model of alternating hemiplegia of childhood: behavioral and electrophysiologic characterization.Epilepsia, vol. 56, no. 1, Jan. 2015, pp. 82–93. Pubmed, doi:10.1111/epi.12878. Full Text

Wang, Liangli, et al. “Neuron-specific Sumo1-3 knockdown in mice impairs episodic and fear memories.J Psychiatry Neurosci, vol. 39, no. 4, July 2014, pp. 259–66. Pubmed, doi:10.1503/jpn.130148. Full Text

Gaier, E. D., et al. “In vivo and in vitro analyses of amygdalar function reveal a role for copper.J Neurophysiol, vol. 111, no. 10, May 2014, pp. 1927–39. Pubmed, doi:10.1152/jn.00631.2013. Full Text

Pages