How your brain seduces you into thinking cigarettes aren't gross
A new study explains why the initial revulsion to cigarettes doesn't last.
Whether you smoke them or not, cigarettes taste nasty — some compare it to licking a burning newspaper, or swallowing ash (yum). But while the majority of people say their first puff tasted terrible, many go on to become addicted anyway. Which begs the question: Why do we do this to ourselves?
If you feel like your body must be betraying you in some way, you might not be far off the mark. Smoking repeatedly may be changing your brain, turning that initial ‘ugh’ feeling into something you just can’t go without, according to a new study.
The research is the first to consider how neurons that signal aversion are affected by an addiction to cigarettes, and points towards the possibility of future smoking cessation therapies.
The findings are due to be published in the Proceedings of the National Academy of Sciences this week.
Why cigarettes taste so bad — at first
Previously, it was thought that the disgust associated with that first cigarette was driven by nicotine, which can stimulate both pleasure and aversion neurons in the brain. But the new results suggest that when a person smokes for the first time, both reward and aversion brain cells are activated. These sensations link back to two populations of brain cells found in the ventral tegmental area (VTA) of the brain, part of the reward system.
Taryn Greider, a scientist at the University of Toronto and author on the study, tells Inverse that the main things that lead to smoking feeling good or bad are an increase in the number of receptors in our brains and a change in how the different structures in the brain communicate with each other.
Greider and her team found that in mice bred to feel indifferent to nicotine, smoking changes the number of aversion receptors in the brain and alters their signaling. They then infected the mice with a virus that introduced nicotine receptors in an area of the VTA dominated by two types of neurons — dopamine and GABA neurons.
The researchers then dose the mice with nicotine and scanned their brains while simultaneously observing their behavior. The mice’s dopamine neurons triggered nicotine aversion — while the GABGA neurons triggered the feeling of reward.
People generally think of dopamine as a reward chemical, but it is more of a motivation signal, says Greider. When it’s active, it increases the motivation to do anything — rewarding or not.
“Here we showed that it leads to the motivation to avoid nicotine,” she says.
The problem with dopamine
But dopamine’s motivational trigger can work in the opposite way, too, Greider says. “We have also showed that the pattern of dopamine activity signals the bad feelings of withdrawal, and the motivation to avoid it.”
As the mice became addicted to nicotine, the dopamine neurons began to signal both reward and aversiveness. The aversive signals become weaker over time, boosting the reward signal. Eventually, the mice seem to only feel reward — and avoid withdrawal instead of the nicotine itself.
Understanding how aversion switches to reward may help develop therapies that capitalize on the disgusting aspects of smoking, even in long-time smokers, Greider says.
“If we can eventually develop a drug treatment that shuts down the rewarding brain cells but leaves the sense of disgust active, then when a person smokes they will only feel disgust and they would hopefully be helped to quit forever,” she says.
Evidence shows that the neurotransmitter dopamine mediates the rewarding effects of nicotine and other drugs of abuse, while nondopaminergic neural substrates mediate the negative motivational effects. β2 nicotinic acetylcholine receptors (nAChR) are necessary and sufficient for the experience of both nicotine reward and aversion in an intra-VTA (ventral tegmental area) selfadministration paradigm. We selectively reexpressed β2 nAChRs in VTA dopamine or VTA γ-amino-butyric acid (GABA) neurons in β2−/− mice to double-dissociate the aversive and rewarding conditioned responses to nicotine in nondependent mice, revealing that β2 nAChRs on VTA dopamine neurons mediate nicotine’s conditioned aversive effects, while β2 nAChRs on VTA GABA neurons mediate the conditioned rewarding effects in place-conditioning paradigms. These results stand in contrast to a purely dopaminergic reward theory, leading to a better understanding of the neurobiology of nicotine motivation and possibly to improved therapeutic treatments for smoking cessation.