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

Daigle, Tanya L., et al. “Opposite function of dopamine D1 and N-methyl-D-aspartate receptors in striatal cannabinoid-mediated signaling..” Eur J Neurosci, vol. 34, no. 9, Nov. 2011, pp. 1378–89. Pubmed, doi:10.1111/j.1460-9568.2011.07874.x. Full Text

Cohen, Sonia, et al. “Genome-wide activity-dependent MeCP2 phosphorylation regulates nervous system development and function..” Neuron, vol. 72, no. 1, Oct. 2011, pp. 72–85. Pubmed, doi:10.1016/j.neuron.2011.08.022. Full Text

Bhatia, Kamal S., et al. “Reversal of long-term methamphetamine sensitization by combination of pergolide with ondansetron or ketanserin, but not mirtazapine..” Behav Brain Res, vol. 223, no. 1, Sept. 2011, pp. 227–32. Pubmed, doi:10.1016/j.bbr.2011.04.045. Full Text

Wang, Xiaoming, et al. “Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3..” Hum Mol Genet, vol. 20, no. 15, Aug. 2011, pp. 3093–108. Pubmed, doi:10.1093/hmg/ddr212. Full Text

Porton, Barbara, et al. “Synapsin III: role in neuronal plasticity and disease..” Semin Cell Dev Biol, vol. 22, no. 4, June 2011, pp. 416–24. Pubmed, doi:10.1016/j.semcdb.2011.07.007. Full Text

Carlson, Benjamin R., et al. “WRP/srGAP3 facilitates the initiation of spine development by an inverse F-BAR domain, and its loss impairs long-term memory..” J Neurosci, vol. 31, no. 7, Feb. 2011, pp. 2447–60. Pubmed, doi:10.1523/JNEUROSCI.4433-10.2011. Full Text

Rodriguiz, Ramona M., et al. “Neurophenotyping genetically modified mice for social behavior..” Methods Mol Biol, vol. 768, 2011, pp. 343–63. Pubmed, doi:10.1007/978-1-61779-204-5_19. Full Text

Wetsel, William C. “Hyperthermic effects on behavior..” Int J Hyperthermia, vol. 27, no. 4, 2011, pp. 353–73. Pubmed, doi:10.3109/02656736.2010.550905. Full Text

Wetsel, William C. “Sensing hot and cold with TRP channels..” Int J Hyperthermia, vol. 27, no. 4, 2011, pp. 388–98. Pubmed, doi:10.3109/02656736.2011.554337. Full Text

Gaier, Eric D., et al. “Haploinsufficiency in peptidylglycine alpha-amidating monooxygenase leads to altered synaptic transmission in the amygdala and impaired emotional responses..” J Neurosci, vol. 30, no. 41, Oct. 2010, pp. 13656–69. Pubmed, doi:10.1523/JNEUROSCI.2200-10.2010. Full Text

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