Adolescents are uniquely susceptible to nicotine’s rewarding and reinforcing effects. Moreover, their immature cognitive control and impulsive behavior make them more likely to experiment with vaping and escalate their tobacco use.
Scientists are concerned that exposing teenagers to nicotine can have long-term consequences. It is because the brain continues to develop until about age 25, and drug exposure can affect this development.
1. Adolescent Brain Development
Adolescence is a time of significant reorganization of forebrain circuitry. During this developmental period, the brain is susceptible to new experiences with significant experience-dependent plasticity in executive control and decision-making regions, including the prefrontal cortex. That makes adolescent brains vulnerable to risk-taking and novelty-seeking behavior.
It is also a time of increased vulnerability to drug abuse. Adolescents are more likely to initiate alcohol and nicotine use than adults. Furthermore, they are more likely to escalate their cigarette and e-cigarette use once they start and may begin experimenting with other illegal drugs.
Research has shown that adolescent brains are more susceptible to the effects of nicotine than adult brains. In animal studies, nicotine increases locomotor activity and the expression of c-fos mRNA in sensory and limbic cortices more robustly in adolescents than in adult rats. Similarly, nicotine administration reduces the accuracy of correct stimulus detection and increases premature and time-out responses compared to controls in a visuospatial attentional task. These deficits are consistent with impaired attention and impulsiveness, which are hallmarks of addiction.
Another unique effects of smoking on the teenage brain is its impact on monoamine neurotransmitters, especially dopamine. Nicotine increases the sensitivity of dopamine neurons in the ventral tegmental area to regulation by glutamate via mGluR2 receptors.
Interestingly, it also enhances the activity of layer V pyramidal neurons in the PFC, which handle diverse incoming information from the mediodorsal thalamus and local neurons to NMDA receptor activation. This altered activity may compromise the ability of these neurons to filter out irrelevant sensory information.
2. Adolescent Smoking
The adolescent period is a time of enhanced vulnerability to drug-related disorders. Research at clinical and preclinical levels indicates that this sensitivity is related to immature neurobiology. Adolescence is a time of rapid reorganization in brain regions that control cognition, reward processing, and emotion. Nicotinic acetylcholine receptors regulate the maturation of these areas. Hence, adolescent exposure to nicotine has long-term consequences for adolescent brain development.
In addition to its effect on the limbic system, nicotine also influences the prefrontal cortex (PFC). This area is critical for attention, working memory, and cognitive flexibility. Studies have found that chronic nicotine exposure alters how layer V pyramidal neurons in the PFC process diverse incoming information from the mediodorsal thalamus. Specifically, it reduces short-term plasticity in this region and negatively impacts their ability to filter out irrelevant sensory information.
Moreover, the prefrontal cortex is a crucial component of the neural circuitry that mediates decision-making and response to stressors. It is well established that smoking during adolescence increases impulsiveness and risk-taking, which can have severe consequences for one’s health. These responses are driven mainly by cholinergic projections from the ventral tegmental nucleus and the nucleus accumbens.
Recent studies indicate that adolescent exposure to nicotine modulates these dopamine signaling pathways. Specifically, it decreases the binding of dopamine transporters in these regions and increases the striatal release of serotonin. This mechanism explains the heightened vulnerability of adolescents to nicotine’s rewarding effects.
3. Adolescent Addiction
Adolescence is a vulnerable period of enhanced clinical vulnerability to nicotine and other drug abuse. It is due to a combination of sociocultural factors and preclinical and clinical studies demonstrating a unique neurobiological basis for this sensitivity. The adolescent brain is susceptible to perturbations of cholinergic systems that regulate cognitive and executive function, working memory, and reward processing. Nicotinic acetylcholine receptors regulate these systems, and disruption of nAChRs in adolescence has long-term consequences for mental health and addiction.
Addiction to nicotine and other drugs can lead to various behavioral problems. The brain’s “reward” circuit becomes impaired, resulting in a craving for more and more of the drug. Addiction can also alter a teen’s personality and behavior, leading to irresponsible decisions, unhealthy or destructive behaviors, and even social isolation.
Many adolescents become addicted to drugs to deal with difficult emotions, such as anxiety, depression, anger, or fear. The reward system in the brain is activated by these feelings, which causes the drug to give the teen a feeling of pleasure or euphoria. However, this temporary feeling is insufficient to deal with the real problem. In addition, the brain’s frontal cortex is not fully developed during adolescence, which makes them easily influenced by peer pressure, and they are often more likely to take risks with negative consequences.
4. Adolescent Mental Health
Nicotine is a chemical found in tobacco products like cigarettes, chewing tobacco, and e-cigarettes. When smoked or vaporized, nicotine enters the brain and activates reward pathways to produce feelings of pleasure. In addition, nicotine changes how the brain responds to stress and lowers impulse control. That is why young people are particularly susceptible to nicotine addiction and mood disorders. The brain’s parts that help them handle stress, learn effectively, and exhibit self-control still develop during adolescence.
Adolescents progress faster to nicotine dependence, find nicotine more rewarding, and are likelier to underestimate the health risks of smoking. It makes the adolescent brain uniquely vulnerable to the effects of nicotine.
Conclusion
Studies also show that adolescent, but not adult, nicotine exposure causes unique and persistent deficits in visuospatial attentional tasks and serial pattern learning. These deficits may be related to changes in striatal dopamine transporters and long-term potentiation of cocaine behavioral responses in the nucleus accumbens shell.
Moreover, nicotine alters how the brain develops new cells and synapses. It means that the brains of teens who smoke or vape develop more receptors for nicotine and require more of it to produce the same pleasurable effect. It leads to nicotine addiction and mood disorders like depression or anxiety.
