|Study Identifies Key Gene in Nicotine's Reward Effect|
Changes in dopamine system signaling result in long-lasting effects on brain
WEDNESDAY, Dec. 6 (HealthDay News) -- Yale University researchers say they've spotted a gene that plays an important role in how nicotine affects the brain.
In research with mice, the team found that nicotine can increase the activity of a molecule called CREB in a brain area called the nucleus accumbens. CREB can alter the properties of nerve cells, an action that's key in nicotine's rewarding effects in the brain.
Introducing a genetically altered virus that blocks CREB activity in the nucleus accumbens blocked that nicotine reward, the researchers found.
The study, funded by the U.S. National Institute on Drug Abuse, was presented Tuesday at the annual meeting of the American College of Neuropsychopharmacology, in Nashville, Tenn.
"We and other researchers have begun to make very strong links between individual molecules in the brain and nicotine-related behaviors. By identifying molecules and changing their activity, we can understand how overall behavior is changed," researcher Marina Picciotto, associate professor of psychiatry, said in a prepared statement.
Nicotine activates the dopamine system in the brain. Dopamine is a neurotransmitter that plays a key role in motivation and reward processes. Drugs such as cocaine and amphetamines also activate the dopamine system.
"Our work and that of others has shown that nicotine changes signaling in nerve cells in the dopamine system resulting in long-lasting effects. We believe that these changes in signaling may explain why people who quit smoking can continue to experience cravings many years later or even start smoking again," Picciotto said.
This line of research may help identify new targets for treatments to help people stop smoking, the researchers said.
The American Cancer Society offers a guide to quitting smoking.
Copyright © 2002 ScoutNews, LLC. All rights reserved.
SOURCE: American College of Neuropsychopharmacology, news release, Dec. 5, 2006