Treatment studies provide minimal support for nicotine replacement therapy (NRT) with youth; however, survey studies suggest that adolescents use NRT, and may engage in inappropriate use. The current study sought to examine patterns of NRT use and risk factors for use to further aid smoking cessation efforts including prevention of potential misuse. In-school surveys assessing socio-demographic and behavioral factors associated with NRT use, gum or patch, were completed by 4078, predominantly African American, high school students. Approximately 5% of students reported former or current use of NRT products: 42% gum, 29% patch, and 29% both gum and patch. Among smokers, 5.4% reported use of both NRT gum and patch, with exclusive use of gum twice as likely as exclusive use of the patch. Those with high-risk-taking attitudes were more likely than low-risk takers (3% vs. 1%) to report use of both products, with exclusive gum use more prevalent than patch use. A cumulative logit model revealed males, risk takers, and/or smokers were at greatest odds for NRT use. Among this adolescent sample, NRT gum was used more often than the patch. Adolescent males, risk takers, and/or smokers appear more likely to use NRT (gum and/or patch) compared to their counterparts, despite limited empirical support for effective use of these products as cessation aids among adolescents. Smoking cessation and prevention programs may emphasize appropriate NRT use, specifically within these populations.

The perinate is particularly risk-prone to chemical species which have the potential of inducing neuronal apoptosis or necrosis and thereby adversely altering development of the brain, to produce life-long functional and behavioral deficits. This paper is an overview for many substances of abuse, but the purview is much more broadened by the realization that even elevated levels of estrogens and corticosteroids in the pregnant mother can act as neuroteratogens, by passing via the placenta and altering neural development or inducing apoptosis in the perinate. Finally, therapeutic risks of anesthetics are highlighted, as these too induce neuronal apoptosis in the neonate by either blocking N-methyl-D-aspartate receptors or by acting as gamma-aminobutyric acid agonists. By understanding the mechanisms involved it may ultimately be possible to interrupt the mechanistic scheme and thereby prevent neuroteratological processes.

Adolescence is a transitional period between childhood and adulthood, in which the individual undergoes significant cognitive, behavioral, physical, emotional, and social developmental changes. During this period, adolescents engage in experimentation and risky behaviors such as licit and illicit drug use. Adolescents' high vulnerability to abuse drugs and natural reinforcers leads to greater risk for developing substance use disorders (SUDs) during adulthood. Accumulating evidence indicates that the use and abuse of licit and illicit drugs during adolescence and emerging adulthood can disrupt the cholinergic system and its processes. This review will focus on the effects of peri-adolescent nicotine and/or alcohol use, or exposure, on the cholinergic system during adulthood from preclinical and clinical studies. This review further explores potential cholinergic agents and pharmacological manipulations to counteract peri-adolescent nicotine and/or alcohol abuse.

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The purpose of this study was to determine how to best motivate smokers with schizophrenia or schizoaffective disorder to seek treatment for tobacco dependence. Smokers with schizophrenia or schizoaffective disorder (N=78) were randomly assigned to receive a Motivational Interviewing, Psychoeducational, or Minimal Control intervention. A greater proportion of participants receiving the Motivational Interviewing intervention followed through on a referral for tobacco dependence treatment within one-week and one-month post-intervention. Mixed model Analyses of Variance found no differences between groups at one-week or at one-month with respect to tobacco use or motivation to quit. Within group analyses indicated that participants in the Motivational Interviewing and Psychoeducational groups reported significant decreases in cigarettes smoked per day. Only participants in the Motivational Interviewing group showed significant increases in confidence in their ability to quit smoking.

Indiana University-Purdue University Indianapolis (IUPUI) / Tooth decay is a complex dieto-bacterial disease with an association of social, behavioral and biological factors. Streptococcus mutans plays a major role in tooth decay. This endogenous oral microorganism adheres to tooth surfaces and grows and develops into micro-communities that mature and form dental biofilm. Development of cariogenic biofilm is one of the major factors associated with the tooth decay process. The use of tobacco is considered a great risk factor for oral diseases. Several studies demonstrated the association of tooth decay and the use of tobacco as effects of first-hand or second- hand smoking. Nicotine has been reported to increase the biofilm growth and metabolism of S. mutans in a dose-dependent manner up to 16 mg/ml of nicotine. However, its effects on biofilm formation of S. mutans strains isolated from smokers are not known and should be investigated. Therefore, we proposed the use of an in-vitro model to better understand the effects of nicotine on biofilm formation of strains of S. mutans isolates from smokers versus non-smoking subjects. Objectives: To investigate the effects of nicotine on biofilm formation of S. mutans isolates from oral washes of smoker and non-smoker human subjects. Materials and Methods: This study was conducted using three S. mutans isolates collected from oral washes of 10 smoking subjects and 10 non-smoking subjects. The oral wash samples were stored at -80oC before S. mutans isolation. S. mutans isolates were obtained by plating on Mitis Salivarius Sucrose Bacitracin plates and species identity confirmed by carbohydrate fermentation assays. Nicotine from Sigma-Aldrich (St. Louis, MO, USA) was used. Biofilm was formed by overnight culturing of each S. mutans strain (10 μl) in 190 μl of tryptic soy broth (TSB) supplemented with 1.0-percent sucrose (TSBS) containing 0 mg/ml, 0.25 mg/ml, 0.5 mg/ml, 1.0 mg/ml, 2.0 mg/ml, 4.0 mg/ml, 8.0 mg/ml, 16.0 mg/ml, and 32.0 mg/ml of nicotine for 24 hours in 5.0-percent CO2 at 37oC in sterile (8 x 12) 96-well microtiter plates (Fisher Scientific, Newark, DE, USA). The absorbance values of biofilm were measured at 490 nm in a microplate spectrophotometer (SpectraMax 190; Molecular Devices, SunnyVale, CA, USA) after crystal violet staining. Null Hypotheses: 1) Nicotine will not increase biofilm formation in both smoker and non-smoker S. mutans isolates. 2) An increase in nicotine concentrations will not increase biofilm formation in both smoker and non-smoker S. mutans isolates in a dose-dependent manner. 3) Nicotine will not produce significant differences in biofilm formation between smoker and non-smoker S. mutans isolates. Alternative Hypotheses: 1) Nicotine increases the growth of biofilm formation in both smoker and non-smoker S. mutans isolates. 2) An increase in nicotine concentrations increase biofilm formation of both smoker and non-smoker S. mutans isolates in a dose-dependent manner. 3) However, nicotine increases biofilm formation of smoker S. mutans strains more than non-smoker S. mutans isolates. The rationale for this hypothesis is that our preliminary data indicated that S. mutans can become resistant to increased nicotine concentrations and that this resistance appears to be stable and may allow the smoker isolates to be able to respond more vigorously to higher nicotine concentrations than the non-smoker isolates. Results: There was a significant effect (p < 0.05) of both nicotine concentrations and smoking on the growth of biofilm, planktonic cells, and total absorbance, for all strains of S. mutans (p < 0.0001). Isolates from smokers had significantly more biofilm at 0 mg/ml to 16 mg/ml of nicotine compared with those from non-smokers (p-value < 0.0001). Conclusion: S. mutans smoker isolates are more affected by high nicotine concentrations than non-smoker isolates.

Indiana University-Purdue University Indianapolis (IUPUI) / Alcohol use disorder (AUD) and nicotine dependence often result in serious health problems and are top contributors to preventable deaths worldwide. Co-addiction to alcohol and nicotine is the most common form of polysubstance abuse. Epidemiological studies indicate that more than 80% of individuals diagnosed with AUD concurrently use nicotine. The prevalence of alcohol and nicotine comorbidity may stem from interconnected mechanisms underlying these disorders. A better understanding of how these drugs interact and the biological basis behind the high comorbidity rates could generate key targets for the development of more effective treatments for AUD and nicotine dependence. The following experiments utilized four similar overall groups consisting of vehicle, ethanol (EtOH), nicotine (NIC), and EtOH+NIC. Chapter Two investigated the efficacy of naltrexone and varenicline, the pharmacological ‘gold standards’ for treating AUD and nicotine dependence, on voluntary drug intake by rats selectively bred for high EtOH drinking. The results indicated that the standard treatments for AUD and nicotine dependence were effective at reducing consumption of the targeted reinforcer but neither reduced EtOH+NIC co-use/abuse. Chapter Three examined the effects of peri-adolescent EtOH drinking on the ability of NIC infused into the posterior ventral tegmental area (pVTA) to stimulate dopamine release within the nucleus accumbens (NAc) shell during adulthood. The results suggest a cross-sensitization to NIC produced by peri-adolescent EtOH consumption demonstrated by a leftward and upward shift in the dose response curve. Chapter Four investigated the effects of intra-pVTA infusions on NAc shell neurochemistry, EtOH reward within the NAc shell, and the role of brain-derived neurotrophic factor (BDNF) on EtOH reward within that region. The data indicated that only EtOH+NIC significantly increased glutamate, dopamine, and BDNF in the NAc shell. Repeated pretreatment with EtOH+NIC also enhanced EtOH reward in the NAc shell and BDNF infusions were sufficient to recapitulate these findings. Collectively, the data indicate that concurrent exposure to EtOH and NIC results in unique neuroadaptations that promote future drug use. The failure to develop effective pharmacotherapeutics for AUD or nicotine dependence could be associated with examining potential targets in models that fail to reflect the impact of polydrug exposure. / 2020-04-03

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Rationale. Alcohol use disorders (AUDs) and tobacco dependence are frequently identified as co-morbid. Although less than 20% of the general population smokes, over 80% of people with AUDs are considered daily smokers. In fact, people with AUDs are more likely to die from smoking-related health issues, than from alcohol related health issues. Surprisingly, there is very little evidence that alcohol and nicotine are concurrently self-administered in pre-clinical models. We hypothesized that low doses of nicotine that enhancing responding for other rewards would be self-administered and enhance self-administration of alcohol. Objective. The goal of this study was to determine if low-doses of nicotine, typically not self-administered alone, would promote alcohol self-administration in a concurrent access paradigm. Method. Alcohol preferring rats (females) were requested from the University of Indiana Medical School breeding facility. They were randomly assigned to one of three groups – NIC-Alone, ALC-Alone, or ALC+NIC. All rats were fluid restricted and shaped to lick for water at two sipper tubes that could record lick responses and deliver aliquiots of fluid into the sipper tube via a solenoid valve. After shaping, rats were instrumented for IV self-administration. During self-administration tests, rats in the ALC-Alone received access to oral ethanol (15% v/v) for meeting the schedule of reinforcement at one sipper tube (e.g., right) and saline infusions for meeting the schedule of reinforcement at the other sipper tube (e.g., left). The NIC-Alone group received IV nicotine infusions (15 ug/kg/inf) and oral licorice (1%) for meeting the schedule of reinforcement at one sipper tube (e.g., left) and oral water for meeting the schedule of reinforcement at the other sipper tube (e.g., right). The ALC+NIC group received IV nicotine and oral licorice for meeting the schedule of reinforcement on the left sipper, and oral ethanol for meeting the schedule of reinforcement on the right sipper. Price manipulations for nicotine were performed by adjusting the schedule of reinforcement on the sipper associated with nicotine infusions. Results. During acquisition, nicotine did not enhance alcohol self-administration – alcohol intake was comparable between ALC-Alone and ALC+NIC rats. In addition, alcohol did not enhance nicotine self-administration as responding for NIC was comparable between ALC+NIC and NIC-Alone rats. However, when the price of nicotine was manipulated, alcohol created a greater demand for nicotine, as indicated by higher rates of nicotine consumption with increases in price. Manipulating the price of nicotine did not alter demand for alcohol. Conclusion. The interaction between alcohol and nicotine reinforcers may depend on changes in demand for nicotine. Future studies should investigate whether demand for alcohol is altered by concurrently available nicotine infusions. *the first and second authors contributed equally to this project