Do receptors mediate the effects of nicotine on anxiety?
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Cigarette smoking has led to an epidemic of lung cancer and heart disease, costing billions of dollars in health care as the major preventable cause of poor health in the United States. In California alone, the cost of smoking on health care reached nearly $16 billion in 1999. Although major efforts have been made to educate people about the health risks associated with smoking and encourage people to stop smoking, millions of Americans continue to smoke. One factor that may contribute to the persistence of smoking is anxiety. During stressful or anxious periods, smokers smoke more heavily and report decreased levels of anxiety following tobacco consumption. It is also during these times of heightened stress or anxiety that those who have quit often start smoking again. In addition, increased anxiety is commonly observed during the first few weeks after stopping smoking. While cigarette smoking is a complex addiction, these findings suggest that smoking may continue as a means of coping with anxiety. If the effects of smoking on anxiety are better understood, we may be able to provide better drugs and/or therapies to help cope with life’s stress that could disrupt the cycle of nicotine dependence and discontinue this life-threatening habit. 
 
 
 
 
 
 
 
 Among the many components of cigarette smoke, nicotine has been shown to be the primary addictive substance. Nicotine acts in the body by binding to a group of proteins called nicotinic receptors. There are many types of nicotinic receptors in the brain, although we do not yet know what each type does. Some types of nicotinic receptors, however, have been found in regions known to be involved in addiction for many drugs such as cocaine, heroin and amphetamine, suggesting that these receptors may mediate addiction to nicotine. To investigate whether one of these nicotinic receptor types, those containing the beta3 subunit, are involved in nicotine addiction, we made an animal model that does not express beta3. By studying behaviors associated with nicotine addiction in this animal model, we can determine whether beta3 nicotinic receptors are involved in these behaviors. We have already found that our animal model lacking the beta3 subunit shows lower levels of anxiety, suggesting that beta3 receptors regulate some forms of anxiety. Therefore, we hypothesize that the effects of nicotine on anxiety reported by smokers may be regulated by beta3 nicotinic receptors. 
 
 
 
 
 
 If these studies confirm that increased nicotine consumption following stress is mediated by beta3 nicotinic receptors, these data would suggest that beta3 receptors may be responsible for the increased smoking observed in human smokers after stress or anxiety. If that is the case, drugs designed to bind specifically to beta3 nicotinic receptors that interfere with increased smoking during times of stress may greatly aid in the effort to stop smoking.