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

Molecular and circuitry mechanism underlying autism behaviors in Shank3 mouse models awarded by National Institutes of Health (Co Investigator). 2019

Cortico-striatal neurotransmission and compulsive motor behaviors awarded by National Institutes of Health (Co Investigator). 2008 to 2019

Initial SHANK3 Study (Rugen E & F) awarded by Rugen Holdings (Cayman) (Principal Investigator). 2017 to 2019

Initial SHANK3 Study awarded by Rugen Holdings (Cayman) (Principal Investigator). 2016 to 2019

Linking Ciliary Biology to the Functional Annotation of Psychiatric Disorders awarded by University of Nevada - Las Vegas (Principal Investigator). 2018

Quantitative MR Microscopy of Phenotypic Biomarkers in Alzheimer's Disease awarded by National Institutes of Health (Co-Mentor). 2013 to 2018

Analysis of Shank3 Complete and Temporal and Spatial Specific Knockout Mice awarded by National Institutes of Health (Collaborator). 2012 to 2018

Receptor Regulation of CCK Cell Function awarded by National Institutes of Health (Consultant). 2013 to 2018

IPA - Jiechun Zhou awarded by National Institutes of Health (Principal Investigator). 2017 to 2018

IPA - William Wetsel awarded by National Institutes of Health (Associate Research Professor). 2017 to 2018

Pages

Berezniuk, Iryna, et al. “ProSAAS-derived peptides are regulated by cocaine and are required for sensitization to the locomotor effects of cocaine.J Neurochem, vol. 143, no. 3, Nov. 2017, pp. 268–81. Pubmed, doi:10.1111/jnc.14209. Full Text

Pogorelov, Vladimir M., et al. “5-HT2C Agonists Modulate Schizophrenia-Like Behaviors in Mice.Neuropsychopharmacology, vol. 42, no. 11, Oct. 2017, pp. 2163–77. Pubmed, doi:10.1038/npp.2017.52. Full Text

Akkhawattanangkul, Y., et al. “Targeted deletion of GD3 synthase protects against MPTP-induced neurodegeneration.Genes Brain Behav, vol. 16, no. 5, June 2017, pp. 522–36. Pubmed, doi:10.1111/gbb.12377. Full Text

Wang, Jianjun, et al. “G protein-coupled receptor kinase-2 (GRK-2) regulates serotonin metabolism through the monoamine oxidase AMX-2 in Caenorhabditis elegans.J Biol Chem, vol. 292, no. 14, Apr. 2017, pp. 5943–56. Pubmed, doi:10.1074/jbc.M116.760850. Full Text

Urs, Nikhil M., et al. “Distinct cortical and striatal actions of a β-arrestin-biased dopamine D2 receptor ligand reveal unique antipsychotic-like properties.Proc Natl Acad Sci U S A, vol. 113, no. 50, Dec. 2016, pp. E8178–86. Pubmed, doi:10.1073/pnas.1614347113. Full Text

Badea, Alexandra, et al. “The fornix provides multiple biomarkers to characterize circuit disruption in a mouse model of Alzheimer's disease.Neuroimage, vol. 142, Nov. 2016, pp. 498–511. Pubmed, doi:10.1016/j.neuroimage.2016.08.014. Full Text

Ade, Kristen K., et al. “Increased Metabotropic Glutamate Receptor 5 Signaling Underlies Obsessive-Compulsive Disorder-like Behavioral and Striatal Circuit Abnormalities in Mice.Biol Psychiatry, vol. 80, no. 7, Oct. 2016, pp. 522–33. Pubmed, doi:10.1016/j.biopsych.2016.04.023. Full Text

Bhagat, Srishti L., et al. “Mouse model of rare TOR1A variant found in sporadic focal dystonia impairs domains affected in DYT1 dystonia patients and animal models.Neurobiol Dis, vol. 93, Sept. 2016, pp. 137–45. Pubmed, doi:10.1016/j.nbd.2016.05.003. Full Text

Barak, Larry S., et al. “ML314: A Biased Neurotensin Receptor Ligand for Methamphetamine Abuse.Acs Chem Biol, vol. 11, no. 7, July 2016, pp. 1880–90. Pubmed, doi:10.1021/acschembio.6b00291. Full Text

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