William Christopher Wetsel, PhD

Associate Professor in Psychiatry and Behavioral Sciences
Assistant Research Professor in Cell Biology
Assistant Professor in Medicine
Associate Professor in Neurobiology
Faculty Network Member of the Duke Institute for Brain Sciences
Campus mail 354 Sands Bldg, Durham, NC 27710
Phone (919) 684-4574
Email address william.wetsel@duke.edu

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 and Training

  • Ph.D., Massachusetts Institute of Technology, 1983

Publications

Berezniuk, I, Rodriguiz, RM, Zee, ML, Marcus, DJ, Pintar, J, Morgan, DJ, Wetsel, WC, and Fricker, LD. "ProSAAS-derived peptides are regulated by cocaine and are required for sensitization to the locomotor effects of cocaine." Journal of neurochemistry 143, no. 3 (November 2017): 268-281.

PMID
28881029
Full Text

Butler, RK, Ehling, S, Barbar, M, Thomas, J, Hughes, MA, Smith, CE, Pogorelov, VM, Aryal, DK, Wetsel, WC, and Lascelles, BDX. "Distinct neuronal populations in the basolateral and central amygdala are activated with acute pain, conditioned fear, and fear-conditioned analgesia." Neuroscience letters 661 (November 2017): 11-17.

PMID
28916300
Full Text

Pogorelov, VM, Rodriguiz, RM, Cheng, J, Huang, M, Schmerberg, CM, Meltzer, HY, Roth, BL, Kozikowski, AP, and Wetsel, WC. "5-HT2C Agonists Modulate Schizophrenia-Like Behaviors in Mice." Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 42, no. 11 (October 2017): 2163-2177.

PMID
28294132
Full Text

Akkhawattanangkul, Y, Maiti, P, Xue, Y, Aryal, D, Wetsel, WC, Hamilton, D, Fowler, SC, and McDonald, MP. "Targeted deletion of GD3 synthase protects against MPTP-induced neurodegeneration." Genes, brain, and behavior 16, no. 5 (June 2017): 522-536.

PMID
28239983
Full Text

Cho, K-I, Yoon, D, Qiu, S, Danziger, Z, Grill, WM, Wetsel, WC, and Ferreira, PA. "Loss of Ranbp2 in motoneurons causes disruption of nucleocytoplasmic and chemokine signaling, proteostasis of hnRNPH3 and Mmp28, and development of amyotrophic lateral sclerosis-like syndromes." Disease models & mechanisms 10, no. 5 (May 2017): 559-579.

PMID
28100513
Full Text

Wang, J, Luo, J, Aryal, DK, Wetsel, WC, Nass, R, and Benovic, JL. "G protein-coupled receptor kinase-2 (GRK-2) regulates serotonin metabolism through the monoamine oxidase AMX-2 in Caenorhabditis elegans." The Journal of biological chemistry 292, no. 14 (April 2017): 5943-5956.

PMID
28213524
Full Text

Urs, NM, Gee, SM, Pack, TF, McCorvy, JD, Evron, T, Snyder, JC, Yang, X, Rodriguiz, RM, Borrelli, E, Wetsel, WC, Jin, J, Roth, BL, O'Donnell, P, and Caron, MG. "Distinct cortical and striatal actions of a β-arrestin-biased dopamine D2 receptor ligand reveal unique antipsychotic-like properties." Proceedings of the National Academy of Sciences of the United States of America 113, no. 50 (December 2016): E8178-E8186.

PMID
27911814
Full Text

Badea, A, Kane, L, Anderson, RJ, Qi, Y, Foster, M, Cofer, GP, Medvitz, N, Buckley, AF, Badea, AK, Wetsel, WC, and Colton, CA. "The fornix provides multiple biomarkers to characterize circuit disruption in a mouse model of Alzheimer's disease." NeuroImage 142 (November 2016): 498-511.

PMID
27521741
Full Text

Ade, KK, Wan, Y, Hamann, HC, O'Hare, JK, Guo, W, Quian, A, Kumar, S, Bhagat, S, Rodriguiz, RM, Wetsel, WC, Conn, PJ, Dzirasa, K, Huber, KM, and Calakos, N. "Increased Metabotropic Glutamate Receptor 5 Signaling Underlies Obsessive-Compulsive Disorder-like Behavioral and Striatal Circuit Abnormalities in Mice." Biological psychiatry 80, no. 7 (October 2016): 522-533.

PMID
27436084
Full Text

Bhagat, SL, Qiu, S, Caffall, ZF, Wan, Y, Pan, Y, Rodriguiz, RM, Wetsel, WC, Badea, A, Hochgeschwender, U, and Calakos, N. "Mouse model of rare TOR1A variant found in sporadic focal dystonia impairs domains affected in DYT1 dystonia patients and animal models." Neurobiology of disease 93 (September 2016): 137-145.

PMID
27168150
Full Text

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