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Cigarette smokers may be more inclined to crave cocaine, according to a study published this week (November 2) in Science Translational Medicine, which found that the nicotine can result in gene regulation changes that boost the response of mouse brains to the drug.
Scientists have long recognized the trend that drug users tend to start with cigarettes and alcohol before moving on to harder drugs, thus tagging the legal substances with the label "gateway drugs." But there was no mechanism to explain the trend, and the idea has been a continued source of controversy.
In the current study, epidemiologist Denise Kandel at Columbia University, New York, who originally reported on the "gateway drug" idea in 1975, and her husband Eric, a Nobel Prize-winning neurobiologist who spoke with The Scientist just last month about his research, teamed up with other colleagues to see if there was a molecular basis for the theory. The researchers found that mice first treated with nicotine showed enhanced addiction-related behaviors in response to cocaine—specifically, they were 78 percent more likely to go to locations where they had received cocaine previously and 98 percent more active overall. "We found that nicotine works on the DNA-packaging system, known as chromatin," lead author Amir Levine of Columbia told Nature, resulting in the increased expression of drug-addiction-related gene called FosB.
The researchers also analyzed epidemiological data of 1,160 high school students and found that most cocaine users begin using coke after they start smoking, and that smoking increased the risk of addiction to the drug.
"This paper is exciting because it is one of the first well-defined characterizations of gene priming by a drug," neurobiologist Alfred Robison of the Mount Sinai School of Medicine in New York told Nature.