Smoking changes brain
the same way as drugs: study
Reuters, Tuesday, February 20, 2007
WASHINGTON (Reuters) - Smoking causes long-lasting changes in the brain similar to changes seen in animals when they are given cocaine, heroin and other addictive drugs, U.S. researchers said on Tuesday.
A study of the brain tissue of smokers and nonsmokers who had died showed that smokers had the changes, even if they had quit years before, the team at the National Institute on Drug Abuse reported.
"The data show that there are long-lasting chemical changes in the brains of humans," said Michael Kuhar of Emory University in Atlanta, who was not involved in the study.
"The chemical changes alone suggest a physiological basis for nicotine addiction."
A team led by Bruce Hope of NIDA, one of the National Institutes of Health, analyzed levels of two enzymes found inside brain cells known as neurons.
These enzymes help the neurons use chemical signals such as those made by the message-carrying compound dopamine.
Smokers and former smokers had high levels of these enzymes, the researchers reported in the Journal of Neuroscience.
Hope said other studies had seen the same thing in animals given cocaine and heroin -- and it was clear that the drugs were causing the effects.
"This strongly suggests that the similar changes observed in smokers and former smokers contributed to their addiction," he added in a statement.
Experts on smoking have long said that nicotine is at least as addictive as heroin.
The U.S. Centers for Disease Control and Prevention estimates that 20.9 percent of all adults smoke in the United States, which adds up to 45 million people. And 23 percent of high school students smoke.
Brain Changes Persist
Long After Smokers Quit
Washington Post/HealthDay News - Tuesday, February 20, 2007
TUESDAY, Feb. 20 (HealthDay News) -- Smoking produces long-lasting changes in the brains of smokers and former smokers alike, a new study suggests.
For the study, which is published in the Feb. 21 issue ofThe Journal of Neuroscience, researchers from the National Institute on Drug Abuse (NIDA) examined eight samples of human brain tissue from each of three groups: long-term smokers who smoked until death, previous long-term smokers, and nonsmokers. The samples were taken from the nucleus accumbens and the ventral midbrain, two brain regions that play a part in controlling addiction-related behaviors.
All of the participants had died of causes not related to smoking.
The researchers analyzed levels of two specific enzymes found inside brain cells that have been associated with addictive-related behaviors in animals exposed to cocaine, heroin and other illicit drugs.
Levels of these enzymes were elevated in smokers and, more interestingly, former smokers, compared with nonsmokers.
According to lead author Bruce Hope, of NIDA, these findings suggest that the brain changes persist long after smoking has ceased and could contribute to future drug relapse.
"The parallel between the new study and the animal studies is important, because a causal role has been shown in animal studies between increased levels of these neuronal signaling enzymes in these brain regions and addiction-related behaviors. This strongly suggests that the similar changes observed in smokers and former smokers contributed to their addiction," Hope said in a prepared statement.
Hope pointed out that although his findings support previous research, it is not yet clear that these biochemical changes actually cause addiction-related behaviors.
The National Institute on Drug Abuse has more about nicotine addiction.
SOURCE: Society for Neuroscience, news release, Feb. 20, 2007
Long-Term Upregulation of Protein Kinase A and Adenylate Cyclase Levels in Human Smokers
The Journal of Neuroscience, February 21, 2007, 27(8): pages 1964-1972
Bruce T. Hope, Deepti Nagarkar, Sherry Leonard, and Roy A. Wise
Behavioral Neuroscience Branch, Intramural Research Program/National Institute on Drug Abuse/National Institutes of Health/Department of Health and Human Services, Baltimore, Maryland 21224, and 2Department of Psychiatry, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado 80045
Repeated injections of cocaine and morphine in laboratory rats cause a variety of molecular neuroadaptations in the cAMP signaling pathway in nucleus accumbens and ventral tegmental area. Here we report similar neuroadaptations in postmortem tissue from the brains of human smokers and former smokers. Activity levels of two major components of cAMP signaling, cAMP-dependent protein kinase A (PKA) and adenylate cyclase, were abnormally elevated in nucleus accumbens of smokers and in ventral midbrain dopaminergic region of both smokers and former smokers.
Protein levels of the catalytic subunit of PKA were correspondingly higher in the ventral midbrain dopaminergic region of both smokers and former smokers. Protein levels of other candidate neuroadaptations, including glutamate receptor subunits, tyrosine hydroxylase, and other protein kinases, were within normal range.
These findings extend our understanding of addiction-related neuroadaptations of cAMP signaling to tobacco smoking in human subjects and suggest that smoking-induced brain neuroadaptations can persist for significant periods in former smokers.
Key words: cAMP; nicotine; nucleus accumbens; addiction; neuroadaptations; PKA
Received Aug. 23, 2006; revised Jan. 12, 2007; accepted Jan. 18, 2007.
Correspondence should be addressed to Dr. Bruce T. Hope, The National Institute on Drug Abuse, Behavioral Neuroscience Branch, 5500 Nathan Shock Drive, Building C, Baltimore, MD 21224. Email: [url=mailto:firstname.lastname@example.org]email@example.com[/url]
Copyright © 2007 by Society for Neuroscience[/size]