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

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.J Biol Chem, vol. 287, no. 44, Oct. 2012, pp. 37552–63. Pubmed, 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.J Med Chem, vol. 55, no. 16, Aug. 2012, pp. 7141–53. Pubmed, 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

Cawley, Niamh X., et al. “New roles of carboxypeptidase E in endocrine and neural function and cancer.Endocr Rev, vol. 33, no. 2, Apr. 2012, pp. 216–53. Pubmed, doi:10.1210/er.2011-1039. Full Text

Hutchinson, Ashley N., et al. “Differential regulation of MeCP2 phosphorylation in the CNS by dopamine and serotonin.Neuropsychopharmacology, vol. 37, no. 2, Jan. 2012, pp. 321–37. Pubmed, doi:10.1038/npp.2011.190. Full Text

Fukada, Masahide, et al. “Loss of deacetylation activity of Hdac6 affects emotional behavior in mice.Plos One, vol. 7, no. 2, 2012, p. e30924. Pubmed, doi:10.1371/journal.pone.0030924. Full Text

Wong, Peiyan, et al. “Pregnenolone rescues schizophrenia-like behavior in dopamine transporter knockout mice.Plos One, vol. 7, no. 12, 2012, p. e51455. Pubmed, doi:10.1371/journal.pone.0051455. Full Text

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