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Official websites use. Share sensitive information only on official, secure websites. Email: shahrdad uci. Currently, the growing use of tobacco products and electronic cigarettes among teenagers represents a major public health concern. Adolescent exposure to tobacco or nicotine can lead to subsequent abuse of nicotine and other substances, which is known as the gateway hypothesis. Adolescence is a developmentally sensitive time period when risk-taking behaviors, such as sensation seeking and drug experimentation, often begin. These hallmark behaviors of adolescence are largely due to maturational changes in the brain. The developing brain is particularly vulnerable to the harmful effects of drugs of abuse, including tobacco and nicotine products, which activate nicotinic acetylcholine receptors nAChRs. Disruption of nAChR development with early nicotine use may influence the function and pharmacology of the receptor subunits and alter the release of reward-related neurotransmitters, including acetylcholine, dopamine, GABA, serotonin, and glutamate. In this review, we emphasize that the effects of nicotine are highly dependent on timing of exposure, with a dynamic interaction of nAChRs with dopaminergic, endocannabinoid, and opioidergic systems to enhance general drug reward and reinforcement. We present a large collection of clinical and preclinical evidence that adolescent nicotine exposure influences long-term molecular, biochemical, and functional changes in the brain that encourage subsequent drug abuse. Smoking is not only the leading cause of preventable death worldwide, but epidemiological, clinical, and preclinical data have also shown that adolescent exposure to tobacco or nicotine can lead to subsequent abuse of nicotine and other substances. Although previous reports highlight that the rates of cigarette smoking are decreasing in the United States U. This translates to a massive surge of an additional 1. The youth are often attracted to e-cigarettes due to their flavoring, easy availability, and a lack of awareness of their harmful effects. Adolescence is a period of transition characterized by significant hormonal, psychosocial, and neural changes in rodents postnatal day PND 28—42 and humans 12—18 years of age. However, adolescence is also associated with increased vulnerability to stress and risk-taking behaviors, such as sensation seeking and experimentation with recreational drugs. During this sensitive maturational period, the brain is particularly vulnerable to the harmful effects of drugs of abuse, including tobacco and nicotine products. Many factors are recognized to contribute to the onset of teenage substance abuse, such as genetics, stress, and socioeconomic status. We highlight findings from both human and rodent studies, as animal models provide insight into human brain maturation, physiology, and behavior. We performed a thorough review of the literature to characterize impacts of nicotine on the adolescent brain. Nicotine triggers changes in the adolescent brain that alter reward processing and encourage future drug use. Increasing collaboration, resources, and education about the risks of teen nicotine use may contribute to decreases in addiction and drug-related emergencies. The escalation in teenage use of nicotine products prompts the need to raise awareness of the detrimental effects of developmental nicotine exposure. Estimates suggest that drug dependence in the U. The depth of this understanding, specifically the molecular consequences of adolescent nicotine use, allows for individualized treatment plans with a greater emphasis on medication interactions, care coordination, community resources, education, and advocacy. These clinical adjustments may contribute to decreases in addiction and drug-related emergencies. We conducted a comprehensive review of the literature using a two- to three-word combination of the following keywords: adolescence, substance use, nicotinic acetylcholine receptors, gateway, reward, smoking, tobacco, nicotine, alcohol, psychostimulant, cocaine, amphetamine, cannabis, opioids. We utilized the electronic databases of PubMed and Google Scholar for research articles published in English between January and November Articles were included in the review if they discussed nicotine exposure during adolescence, drug sequence patterns, or adolescent substance use. The references from relevant articles and websites of relevant organizations were also examined for other potential sources of information. Out of 80, initial search results, approximately 5, were reviewed as relevant and non-duplicate articles. To retain focus on adolescent initiation of nicotine products, studies related to maternal tobacco or nicotine exposure were excluded. Studies evaluating other interventions i. We grouped studies together according to their methodological similarities, so findings without substantial support or reproducibility i. Following exclusion and careful analysis of studies based on key results, limitations, suitability of the methods to test the initial hypothesis, and quality and interpretation of the results obtained, references were selected. The use of two reviewers and two extensive electronic databases allows for a widespread range of research articles, which maximizes scientific credibility and minimizes potential bias. Drugs of abuse provide rewarding, pleasurable feelings that contribute to its reinforcement i. Although common drugs of abuse, like marijuana, cocaine, alcohol, and opioids, act on different neurotransmitter systems, they all exert their reinforcing effects via the mesolimbic pathway, a dopaminergic pathway that connects the ventral tegmental area to the nucleus accumbens. Substantial epidemiological data suggest that teenagers are more vulnerable than adults to nicotine dependence following minimal tobacco exposure fewer than seven cigarettes in one month , and individuals who begin smoking during adolescence are more likely to experience difficulty quitting than those who start as adults. Animal models allow for experimenter-controlled administration of nicotine and investigation of its direct consequences on the brain and behavior through neuroimaging, biochemical assays, and behavioral tests. Early adolescent rats exposed to intravenous nicotine levels equivalent to one to two cigarettes per day for four days Figure 1 self-administer a greater amount of cocaine, methamphetamine, and alcohol compared to adolescent rats not exposed to nicotine, as well as compared to exposed and unexposed adults. In addition, adolescent, but not adult, rodents exposed to nicotine display disruptions in hippocampal learning, long-lasting depressive phenotypes, changes in cocaine sensitivity and reward, enhanced drug-related learning, and deficits in impulse control, executive function, and cognition. In addition, brief nicotine exposure in early adolescent rats enhances cellular activity, dopamine D2 receptor signaling, and serotonin 5-HT receptor function in brain reward areas compared to adult rats also exposed to nicotine. Two intravenous nicotine 0. Experimentation following nicotine pretreatment dashed lines varies upon the drug administered, duration of drug administration, and contingent or non-contingent injections. PND , postnatal day ; IV , intravenous; mg , milligram; kg , kilogram; ng , nanogram; ml , milliliter. Other drug-associated behaviors are beyond the scope of this review and will not be discussed. The developments of alcohol and tobacco use patterns are closely related among teenagers, but the order of progression is not universal among cultural and ethnic demographics. Adolescent susceptibility to co-use of nicotine and alcohol is also observed in rodents, as concurrent self-administration of both drugs in adolescent, but not adult, rats is reinforcing and leads to an increase in subsequent oral alcohol intake. In humans, adolescent exposure to nicotine influences the likelihood of other psychostimulant use, including cocaine and methamphetamine. S population revealed that the rate of cocaine dependence was highest among cocaine users who initiated cocaine after having smoked cigarettes Preclinical studies also demonstrate associations between adolescent nicotine exposure and psychostimulant consumption. Chronic nicotine exposure differentially alters cocaine-induced locomotor activity and intravenous cocaine self-administration in adolescent versus adult rodents. In addition to the enhanced use of alcohol and psychostimulants following early nicotine use, cigarette smoking in adolescents and young adults is associated with earlier onset of cannabis use, more frequent cannabis use, and a larger number of cannabis use disorder symptoms compared to those who did not smoke cigarettes. Although little research has been done on nAChRs interactions with THC specifically during adolescence, preclinical findings in adults suggest that cholinergic and endocannabinoid systems interact to modulate reward-related processes. The endogenous opioid system is primarily involved in pain relief, reward processing, emotion, stress, and autonomic control, and consists of 3 families of receptors: mu, delta, and kappa. Enkephalins, endorphins, endomorphins, and opioids act primarily through mu opioid receptors MORs to reduce pain perception, while dynorphins preferentially act at kappa opioid receptors KORs to regulate appetite, stress, and emotion. Mu and delta opioid receptors play a critical role in drug reward, whereas the KORs participate in drug aversion. Although opioid use has not been extensively evaluated during adolescence, an abundance of clinical and preclinical evidence suggests an important bidirectional relationship between nicotine use and opioid reward. Activation of nAChRs can influence excitability of opioid-containing neurons, and nicotine-induced dopamine release in the nucleus accumbens is dependent on activation of MORs in the ventral tegmental area. Perhaps unsurprisingly, given the significant overlap of cholinergic and opioidergic systems, clinical data show that treatment with naloxone and naltrexone, both opioid receptor antagonists, reduces tobacco smoking and craving for tobacco smoke. The relationship between nicotine and the opioidergic system is similarly substantial in preclinical studies, which is important given the roles of both systems in reward processing. Early adolescent nicotine exposure in mice enhances subsequent morphine reward. Although there are minimal data on nicotine and opioid interactions during adolescence, increasing evidence supports a role of the KOR system in modulating nicotine-associated behaviors. Rodent studies suggest that teen susceptibility to nicotine use is likely due to adolescents finding nicotine more rewarding and less aversive than adults. We present epidemiological and clinical findings supporting the gateway hypothesis Table 1 , and emphasize that early adolescent nicotine exposure in various rodent models increases the acquisition and intake of nicotine, alcohol, cocaine, and methamphetamine; co-use of nicotine and alcohol; and the rewarding effects of nicotine, cocaine, methamphetamine, and opioids Table 2. Summary of epidemiological and clinical findings supporting the gateway hypothesis. Details of these selected epidemiological and clinical surveys and findings are highlighted, including age, data source, data analysis, and main observation s. Summary of preclinical studies supporting the gateway hypothesis. Rodent studies highlight nicotine pretreatment paradigms and subsequent observations, including nicotine treatment doses, duration of treatment, species used, age of exposure, behavior tests, and main observation s. Nicotine interacts with other neurotransmitter systems and as a result increases the rewarding effects of other drugs by enhanced activation of reward circuitry. Developing brains are incredibly susceptible to long-lasting changes from perturbations during maturation, leading to behavioral changes that continue into adulthood. The prevalence of nicotine use among adolescents and the extensive interactions between nicotinic receptors and drugs of abuse highlight the critical need to better understand how nicotine modulates long-term consequences on brain and behavior related to addiction vulnerability. This comprehensive review was performed to provide insight into how teenage experimentation with nicotine can induce drastic, ongoing consequences on reward and reinforcement of other drugs of abuse. Recognizing adolescent nicotine use as a possible predisposition to addiction to nicotine itself or other substances may decrease illicit drug experimentation and the incidence of drug addiction. Thus, healthcare professionals should take caution when dealing with adolescents with a history of e-cigarette use and continue to inform about its risks. Given the biochemical adaptations as a consequence of adolescent nicotine exposure, physicians may take an individualized approach to treatment and provide additional resources for patients and their families. This increased education and advocacy may improve care coordination and lead to greater adherence to a discharge plan and improved clinical outcomes. Conflicts of Interest : By the West JEM article submission agreement, all authors are required to disclose all affiliations, funding sources and financial or management relationships that could be perceived as potential sources of bias. There are no other conflicts of interest or sources of funding to declare. As a library, NLM provides access to scientific literature. West J Emerg Med. Find articles by Michelle Ren. Find articles by Shahrdad Lotfipour. Open in a new tab. Age Data source and analysis Main observation s Reference s 24—25 years follow-up of former adolescents aged 15—16 years Longitudinal cohort of former New York State high school students, followed from grades 10 and 11 ages Detailed monthly drug use histories were obtained. The following sequence of progression was tested: alcohol, cigarettes, marijuana, other illicit drugs, and prescribed psychoactive drugs. In addition, months of use and non-use of cigarettes and cocaine were identified. Sequence pattern: Cigarettes preceded marijuana use with or without initial alcohol use among women. However, in men, alcohol consistently preceded marijuana use even in the absence of initial cigarette use. Cigarettes preceded other illicit drugs among women, but not among men. Cigarette and cocaine use: Most cocaine users smoked cigarettes before they started using cocaine. In addition, most cocaine users started using cocaine while they were actively smoking cigarettes i. The subjects were interviewed twice, first during —80 and again during — Eighty-nine percent of those interviewed initially were re-interviewed two years later. Cigarette use fell on a cumulative Guttman scale of use with other drugs e. Having tried substances lower on the Guttman scale made one significantly more likely to be using substances higher on the scale two years later. Use of cigarettes during middle or early high school significantly increased the likelihood that the subject would be using other drugs e. Data were analyzed to clarify whether cigarette smoking has any effect on the initiation of illegal drug use. Those who smoked cigarettes before age 15 were up to 80 times more likely to use illegal drugs than those who did not. Cocaine was the drug most likely to be used among young cigarette smokers. The rates of lifetime cocaine dependence were compared among three groups: 1 those who had started to use cocaine after they had started to smoke and before they had stopped smoking, 2 those who had started cocaine use before beginning to smoke; and 3 those who had ever smoked 0— cigarettes. The rate of cocaine dependence was the highest among cocaine users who initiated cocaine after having smoked cigarettes. The rates of dependence were much lower among those who initiated cocaine before smoking or who had ever smoked 0— cigarettes. The relationship between gateway drugs during 11—20 years of age and drug use in adulthood was analyzed using generalized estimating equation regression models. Exposure to marijuana and illegal substances during young adulthood was positively associated with illegal substance and cocaine use. Interactions between the gateway drugs and reporting high depressive symptoms in adolescence or adulthood were associated with increased use of marijuana, illegal drugs, and cocaine in early or young adulthood. Study selection: longitudinal studies reporting odds ratios for cigarette smoking initiation associated with ever use of e-cigarettes or past day cigarette smoking associated with past day e-cigarette use. E-cigarette use was associated with greater risk for subsequent initiation of cigarette smoking and past day cigarette smoking. Students completed surveys at baseline grade 9 and at a month follow-up grade Associations of baseline e-cigarette, hookah, or combustible cigarette use with ever marijuana use initiation , current marijuana use past 30 days , and current dual use of marijuana and tobacco products were examined at the month follow-up. High schoolers who used e-cigarettes or hookah at baseline compared with those who did not were more likely to report initiation and current use of marijuana as well as dual use of tobacco and marijuana. E-cigarette and hookah use at age 14 years was associated with a 3. The use of e-cigarettes, hookah, and combustible cigarettes in early adolescence more than doubled the odds of currently using both tobacco and marijuana by mid-adolescence. PND 86—90 IV self-administration of cocaine 0. PND 60—69 IV self-administration of nicotine 0. Adolescent rats pretreated with nicotine had sensitization to nicotine-induced repetitive motion over the 7-day nicotine treatment period. Adolescent, but not adult, rats had increased amounts of cocaine-induced repetitive motion after nicotine pretreatment. The high dose of nicotine had no effect on methamphetamine intake and neither nicotine dose altered methamphetamine-primed reinstatement. PND 50—57 vs. PND 70—77 CPP for cocaine, morphine, or amphetamine Mice treated with nicotine during early adolescence, but not late adolescence or adulthood, showed an increase in CPP for cocaine, morphine, and amphetamine later in adulthood. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Longitudinal cohort of former New York State high school students, followed from grades 10 and 11 ages Subjects were sampled from eight public schools in Milwaukee, Wisconsin. Years 12—15, 16—17, 18—25, 26—34, 35—49, 50 or over. National Longitudinal Study of Adolescent to Adult health data spanning a year period. Systematic review and meta-analysis of longitudinal studies that assessed initial use of e-cigarettes and subsequent cigarette smoking. Subjects were sampled from 10 public schools in Los Angeles, California. IV self-administration of cocaine 0. Adolescent rats pretreated with nicotine had increased initial acquisition of cocaine, methamphetamine, and ethanol compared to saline-treated adolescents and both saline- and nicotine-treated adults. Adolescent rats pretreated with nicotine had greater reinforced responding for cocaine compared to saline controls and adults. IV self-administration of nicotine 0. Animals exposed to nicotine during periadolescence self-administered more nicotine than vehicle-exposed animals and animals exposed during postadolescence. Adults exposed to nicotine during early but not late adolescence had increased CPP for cocaine, morphine, and amphetamine. Adults exposed to nicotine during early adolescence had enhanced cocaine-induced locomotor sensitization compared to saline-treated animals. Adults exposed to nicotine during adolescence had increased ethanol self-administration and altered GABA transmission and chloride homeostasis in the ventral tegmental area compared to adolescent and adult saline exposure and adult nicotine exposure. Nicotine pretreatment at a higher dose initially suppressed alcohol consumption but stimulated alcohol consumption on repeated treatment. Nicotine increased locomotor activity in all animals. Locomotor activity, IV self-administration of cocaine descending doses of 1. Adult rats exposed to nicotine during early adolescence were sensitized to the locomotor-activating effects of cocaine and self-administered a greater number of cocaine infusions than adolescent rats pretreated with vehicle. Adult rats that received nicotine treatment during adolescence had enhanced preference for cocaine. IV self-administration of methamphetamine 0. Nicotine-exposed versus saline-exposed rats obtained more methamphetamine infusions. PND 70— Mice treated with nicotine during early adolescence, but not late adolescence or adulthood, showed an increase in CPP for cocaine, morphine, and amphetamine later in adulthood.

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