Claire M. Cannon, Ph.D.
Assistant Professor

Schroeder Complex 447

(414) 288-4428

Email

Website: http://cmcannon.net

Education
Ph.D.	Neuroscience Washington State University 1997 to 2000
B.S.	Psychology University of Washington 1993 to 1997

Research Interest

The primary research focus of our lab is the neurobiology of reward and learning in relation to the human diseases of addiction and obesity.  We use genetically-modified (transgenic) mice that lack the ability to make the neurotransmitter dopamine.  Dopamine levels rise in the brain in response to natural rewards, such as food and social interaction.  In response to drugs of abuse, the rise in brain dopamine may be much greater, and dopamine has been hypothesized to mediate both the rewarding and addictive properties of drugs.  This hypothesis is challenged by our demonstration that mice lacking dopamine nevertheless respond to natural rewards.  If dopamine is not required for normal brain reward processes, it may instead be necessary for the ability of animals to direct their behavior towards appropriate goals.  Our immediate research aims are to better characterize the role of dopamine in the response to natural and drug rewards, and in the ability to learn about rewards.

Selected Publications

1. Cannon, C.M. and Palmiter, R.D.  (2003) Reward without dopamine. Journal of Neuroscience. 23: 10827-10831.

2. Cannon, C.M. and Bseikri, M.R. (2004) Is dopamine required for natural reward? (Invited review)  Physiology and Behavior, 81: 741-748.

3. Cannon, C.M., Abdallah, L., Tecott, L.H., During M.J., and Palmiter, R.D. (2004) Dysregulation of striatal dopamine signaling by amphetamine inhibits feeding by hungry mice.  Neuron. 44: 509-520.

4. Cannon, C.M., Scannell, C., and Palmiter, R.D. (2005) Mice lacking dopamine D1 receptors express normal lithium-chloride-induced conditioned taste aversion for salt but not sucrose. European Journal of Neuroscience. 21: 2600-2604.