Gene-Altered Mouse May Provide New Insights To Parkinson's Disease, Substance Abuse And Sch...( DURHAM N.C. -- Researchers at the Ho...)

DURHAM, N.C. -- Researchers at the Howard Hughes Medical Institute at Duke University Medical Center have deleted the gene for a crucial molecular component of a mouse's nervous system and created an animal that, in essence, mimics a person constantly high on illicit drugs.

Marc Caron, a Hughes investigator and professor of cell biology at Duke, said initial studies with the mice already have yielded surprising insights that challenge conventional theories about drug addiction and Parkinson's disease and may provide the first realistic model for testing new treatments for psychiatric disorders.

"We were astonished that a single genetic deletion would have such a profound effect on both biology and behavior," Caron said. "We believe this mouse will provide an ideal model to study addictive behavior and psychiatric disease."

Caron and his colleagues report their findings in the Feb. 15 issue of the journal Nature. Bruno Giros, the study's lead author, Mohamed Jaber, and Sara Jones of the department of cell biology; and R. Mark Wightman, of the department of neurobiology and chemistry at the University of North Carolina at Chapel Hill, also contributed to the research. The study was funded in part by the National Institutes of Health and an unrestricted neuroscience award from Bristol Myers Squibb.

Caron said in an interview that while it may seem a stretch for one genetically engineered mouse to help answer fundamental questions about the mechanism of addictive drugs, Parkinson's disease, and psychiatric disorders, all are linked by a common problem: a malfunction in the body's regulation of dopamine, an essential messenger of the nervous system.

Neurotransmitters such as dopamine, serotonin and adrenaline are chemical messengers that neurons release to their neighbors to signal them to fire nerve impulses or initiate metabolic changes. Because neurotransmitters are so critical to the smooth functioning of the nervous s
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Contact: Karyn Hede George
georg016@mc.duke.edu
919-660-1301
Duke University
29-Apr-1996