According to a recent study at the University of Massachusetts Medical School published in Current Biology, a single group of brain neurons, called the interpeduncular nucleus, can control physical nicotine withdrawal behaviors. These findings in mice suggest that new therapies could be developed targeting this particular group in order to help people trying to quit smoking.
“Quitting smoking is easy. I’ve done it a thousand times”, Mark Twain said. Why is quitting and staying quit hard for so many people? The answer is nicotine, a drug found naturally in tobacco addictive as heroin or cocaine. Over time, a smoker becomes physically and emotionally dependent on nicotine. Withdrawal symptoms can include dizziness, depressive/anxious feelings, irritability, sleep and attention troubles, headaches, tiredness, and increased appetite and weight gain.
Why it is so important, however, to undergo this challenging experience? As it is widely known and confirmed by scientists half of all smokers will die from a smoking-related illness while nicotine addiction is the primary cause of preventable mortality. In the United States, smoking is responsible for nearly 1 of 5 deaths per year, and about 8.6 million people suffer from smoking-related lung and heart diseases.
The Interpeduncular nucleus (IPN) is a group of ovoid neurons, part of the central nervous system with inhibitory function and associated with other brain areas involved in nicotine use and response, as well as feelings of anxiety. In addition, inside the IPN there are numerous nicotinic acetylcholine receptors, the molecular targets of nicotine.
In the present study, the team of Andrew Tapper and Rubing Zhao-Shea from the Brudnick Neuropsychiatric Research Institute wanted to further elucidate IPN’s implication in quitting smoking and the adverse withdrawal symptoms.
They first exposed mice to nicotine through their water for a period of 6 weeks to get them addicted. After taking the nicotine away, the mice started presenting physical and emotional withdrawal symptoms such as scratching, head nods, and body shakes. In other words, researchers observed a generalized irritability and an increase in anxiety levels comparable to humans’ withdrawal manifestations.
When the team examined the brain they revealed abnormally increased activity in the IPN midbrain region. The same brain region was then artificially activated with light stimulation and researchers observed in the mice similar behaviors to nicotine withdrawal, whether they had previously been exposed to nicotine or not. The reverse effect was also possible. Restraining IPN’s activity during nicotine withdrawal (either by the infusion of an antagonist molecule or by the IPN neurotransmission’s blockade) could alleviate nicotine withdrawal symptoms.
Assistant Professor Andrew Tapper pointed out the current interest of addressing comorbidity as “smoking is highly prevalent in people with other substance-use disorders, suggesting a potential interaction between nicotine and other drugs of abuse”. Although further study is needed, these findings even if related to nicotine alone, could be relevant to other forms of addiction.