Relevant bibliographies by topics / Nicotine addiction

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Nicotine addiction'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Nicotine addiction"

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Miller, Norman S., and James A. Cocores. "Nicotine Dependence: Diagnosis, Chemistry, and Pharmacologic Treatments." Pediatrics In Review 14, no. 7 (July 1, 1993): 275–79. http://dx.doi.org/10.1542/pir.14.7.275.

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Columbus brought tobacco to the Old World, and in the following centuries, tobacco smoking spread throughout the world, despite vigorous opposition. The tobacco plant was named Nicotiana tabacum after Jean Nicot, who promoted his belief that the plant had medicinal value. Nicotine, the basic addicting drug contained in cigarettes, may be the deadliest drug known to humans in terms of overall morbidity and mortality. The morbidity and mortality from nicotine addiction is greater than that from World Wars I and II, the Vietnam War, AIDS (Acquired Immune Deficiency Syndrome), and heroin and cocaine addiction combined. Tobacco use is linked to more than 390 000 deaths per year in the United States alone. The powerful lobbying forces of the tobacco industry have managed to keep supplies of nicotine available to the public despite efforts from medical and legal bodies to reduce advertising and educate the public about the adverse consequences of nicotine use. The addictive potential of cigarettes and the extent to which nicotine is the active ingredient in generating and sustaining addiction has been debated. The reasons for the resistance to considering whether nicotine is addictive have origins in attitudes toward addiction. Free will and personal choice have prevailed as explanations for why a 20-cigarette per day smoker will receive more then 70 000 boluses of nicotine per year despite the high rate of morbidity and mortality associated with this drug.
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Sharma, Geeta, and Sukumar Vijayaraghavan. "Nicotinic Receptors: Role in Addiction and Other Disorders of the Brain." Substance Abuse: Research and Treatment 1 (January 2008): 117822180800100. http://dx.doi.org/10.1177/117822180800100005.

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Nicotine, the addictive component of cigarette smoke has profound effects on the brain. Activation of its receptors by nicotine has complex consequences for network activity throughout the brain, potentially contributing to the addictive property of the drug. Nicotinic receptors have been implicated in psychiatric illnesses like schizophrenia and are also neuroprotective, potentially beneficial for neurodegenerative diseases. These effects of nicotine serve to emphasize the multifarious roles the drug, acting through multiple nicotinic acetylcholine receptor subtypes. The findings also remind us of the complexity of signaling mechanisms and stress the risks of unintended consequences of drugs designed to combat nicotine addiction.
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Jia, Wenbin, Ichiro Kawahata, An Cheng, and Kohji Fukunaga. "The Role of CaMKII and ERK Signaling in Addiction." International Journal of Molecular Sciences 22, no. 6 (March 20, 2021): 3189. http://dx.doi.org/10.3390/ijms22063189.

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Nicotine is the predominant addictive compound of tobacco and causes the acquisition of dependence through its interactions with nicotinic acetylcholine receptors and various neurotransmitter releases in the central nervous system. The Ca2+/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) play a pivotal role in synaptic plasticity in the hippocampus. CaMKII is involved in long-term potentiation induction, which underlies the consolidation of learning and memory; however, the roles of CaMKII in nicotine and other psychostimulant-induced addiction still require further investigation. This article reviews the molecular mechanisms and crucial roles of CaMKII and ERK in nicotine and other stimulant drug-induced addiction. We also discuss dopamine (DA) receptor signaling involved in nicotine-induced addiction in the brain reward circuitry. In the last section, we introduce the association of polyunsaturated fatty acids and cellular chaperones of fatty acid-binding protein 3 in the context of nicotine-induced addiction in the mouse nucleus accumbens and provide a novel target for the treatment of drug abuse affecting dopaminergic systems.
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Tomei, Alexander, Joseph Studer, and Gerhard Gmel. "Prosocialness in young males with substance and behavioral addictions." Journal of Behavioral Addictions 10, no. 2 (July 19, 2021): 327–37. http://dx.doi.org/10.1556/2006.2021.00035.

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AbstractBackground and aimsSocial determinants are closely related to addiction, both as a cause and a consequence of substance use and other addictive behaviors. The present paper examines prosocialness (i.e. the tendency to help, empathize, and care for others) among a population of young males. We compared prosocialness across different types of addiction and examined whether prosocialness varied according to the presence of multiple addictions.MethodsA sample of 5,675 young males, aged 19–29 years old (Mean = 21.4; Median = 21), completed a questionnaire that included screening tools to identify addictive behaviors with regards to alcohol, nicotine, cannabis, gambling, and gaming. The questionnaire also included a scale to measure prosocialness.ResultsCompared to a no-addiction control group, the subgroups of young men suffering from behavioral addictions (i.e., gambling and gaming) reported the lowest levels of prosocialness. Respondents with an alcohol addiction also showed lower prosocialness compared to no-addiction controls. By contrast, no significant differences in prosocialness were found between respondents with nicotine disorder or cannabis disorder and the no-addiction controls. Furthermore, the number of addictions had no clear, observable effects on prosocialness. Significant differences were found between the no-addiction control group and the groups reporting one or more addictions, but not between the separate groups reporting one, two, and three or more addictions.Discussion and conclusionsA better understanding of the social dimension affecting young males with addiction, particularly gambling and gaming addictions, may be useful for their prevention and treatment.
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Santoro, Alessia, Carlo Tomino, Giulia Prinzi, Palma Lamonaca, Vittorio Cardaci, Massimo Fini, and Patrizia Russo. "Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer." Recent Patents on Anti-Cancer Drug Discovery 14, no. 1 (March 13, 2019): 39–52. http://dx.doi.org/10.2174/1574892814666190102122848.

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Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis. Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic receptor”, and “addiction” or “COPD” or “lung cancer” were used. </P><P> Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases. </P><P> New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported. Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation. Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.
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Risi, Ella. "Giving Up Nicotine." British Gestalt Journal 7, no. 1 (June 1, 1998): 49–51. http://dx.doi.org/10.53667/acre2841.

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"Abstract: The paper describes nicotine addiction in the context of chemical dependency generally, including differences between nicotine and other addictions. Addiction is related to narcissistic injury of an already narcissistically wounded self. Difficulties and dangers for the therapist working with clients who are addicted are pointed out. Smokers can benefit from employing alternative coping sirakgies in high risk situations, and other cognitive and interpersonal skills. Key words: nicotine, addiction, chemical dependency, narcissistic injury, phenomenology, lifestyle management."
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Li, Du, and Xiaorui Ma. "Effects and Withdrawal of Drug Addiction." Journal of Education, Humanities and Social Sciences 8 (February 7, 2023): 1454–59. http://dx.doi.org/10.54097/ehss.v8i.4502.

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Drug addiction is very common among people. Thousands of people are now suffering from cocaine addiction. Nicotine addiction may be one of the most common in the world, but many people underestimate the health hazards of nicotine. This report, presents nicotine in four parts: harms and addiction; research; conclusions, and further implications. Because nicotine is not like most banned drugs on the market-nicotine cannot be absorbed directly, people must be exposed to nicotine through a certain medium. The most common and intuitive way is through smoking, secondhand smoke, and e-cigarettes. However, most people don’t start smoking because of nicotine addiction, so the authors of this paper conducted experiments on why people start smoking late. Through self-made questionnaires and online experimental surveys, the results showed people were exposed to smoking because of environmental factors, social factors, psychological factors, and so on. People were exposed to nicotine for too long due to their addiction to cigarettes, which evolved into an addiction to nicotine. In the later stage, due to the addictive nature of nicotine, people no longer smoke because of the original addiction to smoking, but because they want to meet the needs of nicotine.
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Korkmaz Aslan, Tuba, and Serap Batı. "Addiction in university students – determining the levels of cigarette, alcohol, substance, game, and Internet addiction." European Journal of Clinical and Experimental Medicine 21, no. 1 (March 2023): 58–67. http://dx.doi.org/10.15584/ejcem.2023.1.8.

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Introduction and aim. This study aims to determine the average addiction levels of university students and the effects of different demographic variables on addiction levels and types. Material and methods. The study included 783 volunteer students in the Seydişehir campus of Necmettin Erbakan University. Data were collected face-to-face using Sociodemographic Information Form, Fagerström Test for Nicotine Dependence (FTND), Cut-off test (CAGE), Digital Game Addiction Scale (DGAS-7), and Internet Addiction Test (IAT). Results. Of the students, 27.7% were using tobacco, 14.8% were using alcohol, 2.6% were using ecstasy, 2.3% were using cannabis, 1.4% were using inhalants, 1% were using pills. FTND, DGAS-7, and IAT mean scores were 3.80±2.55, 12.04±5.57, and 43.56±15.73, respectively, and 21.5% had risky alcohol use. Also, 2.2% were game addicts, 3.8% were internet addicts. Digital game addiction, internet addiction, and nicotine addiction were positively correlated. There was no significant relationship between nicotine and internet addictions. Individuals with risky alcohol use had higher rates of nicotine addiction. Conclusion. Students’ addiction rates were similar to the country in general. Addictions gained in the youth years continue in the following years and bring many health problems. Therefore, it is crucial to include the subject of combating addiction more in university education and increase studies on the subject.
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Changeux, Jean-Pierre. "Nicotinic receptors and nicotine addiction." Comptes Rendus Biologies 332, no. 5 (May 2009): 421–25. http://dx.doi.org/10.1016/j.crvi.2009.02.005.

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Cooper, Skylar Y., and Brandon J. Henderson. "The Impact of Electronic Nicotine Delivery System (ENDS) Flavors on Nicotinic Acetylcholine Receptors and Nicotine Addiction-Related Behaviors." Molecules 25, no. 18 (September 15, 2020): 4223. http://dx.doi.org/10.3390/molecules25184223.

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Over the past two decades, combustible cigarette smoking has slowly declined by nearly 11% in America; however, the use of electronic cigarettes has increased tremendously, including among adolescents. While nicotine is the main addictive component of tobacco products and a primary concern in electronic cigarettes, this is not the only constituent of concern. There is a growing market of flavored products and a growing use of zero-nicotine e-liquids among electronic cigarette users. Accordingly, there are few studies that examine the impact of flavors on health and behavior. Menthol has been studied most extensively due to its lone exception in combustible cigarettes. Thus, there is a broad understanding of the neurobiological effects that menthol plus nicotine has on the brain including enhancing nicotine reward, altering nicotinic acetylcholine receptor number and function, and altering midbrain neuron excitability. Although flavors other than menthol were banned from combustible cigarettes, over 15,000 flavorants are available for use in electronic cigarettes. This review seeks to summarize the current knowledge on nicotine addiction and the various brain regions and nicotinic acetylcholine receptor subtypes involved, as well as describe the most recent findings regarding menthol and green apple flavorants, and their roles in nicotine addiction and vaping-related behaviors.
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Dissertations / Theses on the topic "Nicotine addiction"

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Harrington, Lauriane. "The role of β4-containing nicotinic acetylcholine receptors in nicotine addiction." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066328/document.

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Le tabac est consommé par environ un milliard de personnes. D'après l'Organisation Mondiale de la Santé, le tabagisme est la première cause évitable de mortalité dans le monde, provocant six millions de morts par an. La nicotine est le composant neuro-actif principal dans le tabac, et exerce ses effets neurologiques via une activation directe des récepteurs nicotiniques de l’acétylcholine (nAChR). Ces récepteurs transmembranaires sont composés de sous-unités alpha, ou alpha plus beta, créant une variété de canaux ioniques ligand-dépendants activés par le neurotransmetteur ACh. Les études génétiques chez l’homme ont mis en évidence des variants dans le cluster génomique CHRNA5-CHRNA3-CHRNB4, codant pour les sous-unités α5, α3 et β4, comme facteurs influençant le tabagisme. Cette thèse a étudié le rôle des nAChRs contenant la sous-unité β4 (β4*) dans l’addiction à la nicotine. En collaboration, nous avons montré que les souris déficientes pour la sous-unité β4 (β4 KO), sont moins sensibles aux effets récompensant et aversifs de la nicotine. En générant un lentivirus exprimant la séquence murine d'ADN complémentaire de β4, j’ai pu restaurer son expression dans des régions d’intérêt du cerveau, sur un fond génétique β4KO. Ceci a permis de mettre en évidence le rôle du réseau habénulo-interpedonculaire dans la contribution des β4* nAChRs à la consommation de nicotine. Ceci a également démontré le rôle modulateur de ces récepteurs dans les réponses de la voie mésolimbique à la nicotine, voie centrale dans l'effet renforçant des drogues
Tobacco is consumed by an estimated 1 billion people world-wide. The World Health Organization names tobacco consumption the primary cause of preventable morbidity and mortality, causing six million deaths per year. Nicotine is the principal neuro-active compound in tobacco, and exerts neurological effects by binding to nicotinic acetylcholine receptors (nAChRs). These transmembrane receptors are composed of alpha or alpha plus beta subunits, forming a diverse variety of ligand-gated ion channels endogenously activated by ACh. Human genetic studies have highlighted variants in the CHRNA5-CHRNA3-CHRNB4 genomic cluster, coding for subunits α5, α3 and β4, as altering smoking behaviours. The present thesis investigated the role of β4-containing (β4*) nAChRs in nicotine addiction. In collaboration, we showed that β4 knockout (KO) mice are less sensitive to nicotine reward and nicotine aversion. Generating a lentivirus for the expression of mouse β4 nAChR subunit complementary DNA, I was able to restore receptor expression to brain regions of interest on a KO background, locating the role of β4* nAChR in nicotine reward and aversion to the habenulo-interpedunular pathway. This also demonstrated the receptor’s modulation of nicotinic responses of the mesolimbic system, central hub of drug reinforcement
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Keyworth, Helen. "Nicotine addiction : behavioural and neurochemical mechanisms." Thesis, University of Surrey, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606818.

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Few attempts "to quit smoking are successful, making current interventions relatively ineffective. Evidence shows that exercise decreases nicotine withdrawal symptoms in humans, but the mechanism is unclear. Part of this thesis aimed to explore the mechanisms underpinning the effect of exercise on nicotine withdrawal in both human and animal models of nicotine addiction. The role of perception of exercise intensity was investigated in temporarily abstinent smokers. Perceived and objective moderate intensity exercise and passive waiting all reduced withdrawal symptoms, and salivary cortisol was attenuated compared with pre*abstinence levels, but there was no difference between any of the interventions. These results indicate that exercise may reduce withdrawal by acting as a distraction, but does not preclude biochemical mechanisms from playing a role. Nicotine-treated mice undertaking 2 or 24 hrs/day running wheel access, demonstrated reduced mecamylamine-precipitated withdrawal symptoms compared with sedentary mice, indicating that even a low level of exercise aids in reducing withdrawal symptoms. This was accompanied by a significant increase in hipp05ampal 0.7 nicotinic receptors (nAChRs), implicating the α7 nAChR in a mechanism underlying the effect of exercise in nicotine withdrawal. The effect of nicotine on nAChR and oxytocin receptor (OTR) binding in a mouse model of schizophrenia was investigated using mice with a G72 protein insertion (G72Tg). Nicotine reversed social cognitive deficits in G72Tg mice, associated with attenuation of α7 nAChR and OTR binding in the cingulate cortex by nicotine in G72Tg mice. These results implicate both α7 nAChRs and OTR as targets for the development of pharmacotherapies for the treatment of social and cognitive deficits in schizophrenia. All toghether, the results in this thesis show that the α7 nAChR may be involved in modulating behavioural responses in nicotine addiction. Furthermore, dysregulation of α7 and OT receptors may underlie the mechanism of cognitive and social deficits in schizophrenia.
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Pashmi, Ghazaleh. "Immunotherapy approach to combat nicotine addiction." Thesis, University of Bath, 2004. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419340.

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Smoking is now recognized as the single largest avoidable cause of premature death and disability in Britain and probably the greatest avoidable threat to public health worldwide. There are several therapies available to combat nicotine addiction ranging from psychological therapy to pharmacological interventions such as Nicotine Replacement Therapy. However, success rates for these therapies individually and mixture of therapies together, are still low and can be improved. A new strategy in helping quit rates is immunotherapy. This research project has focused on targeting cotinine, the major metabolite of nicotine, to produce a vaccine as a cessation method. The effect of cotinine on nicotine-evoked dopamine release was first examined using 96-well plate assay in chapter 2. Cotinine was shown to decrease nicotine - evoked dopamine release, probably by desensitising the nAChRs. a6p2*, a4p2 receptor subtypes were implicated, using competitive antagonists. Trans-4-thiol cotinine was produced as a viable derivative and conjugated to ovalbumin in the appendix and chapter 3. Vaccination of rats generated anti-cotinine antibodies, although mid-point titres were low. Improvements were made in chapter 4 which increased the mid-point antibody titres. The improvements included change of carrier molecule to Tenatus Toxoid, allowing for 15 derivative attachments per carrier molecule, and change of adjuvant. The best concentration of conjugate to be used in vaccination was determined to be 5 pg which produced specific antibodies towards cotinine. Blood nicotine and cotinine concentrations after chronic nicotine treatment showed vaccination resulted in the retention of cotinine in the blood, presumably reducing the concentration reaching the brain, in chapters 4 and 5. Similar results were also obtained after acute nicotine treatment in chapter 5. The effect of vaccination on nicotine - evoked dopamine release was studied in chapters 4 and 5; an increase in nicotine-evoked dopamine release was observed in vaccinated animals. This suggests the retention of cotinine in the blood and the consequent reduction of antagonism of the actions of nicotine by cotinine, allowed nicotine to have a larger effect. Nicotineinduced locomotor activity was not affected by vaccination, however future work is needed to give conclusive results. These results have provided preliminary proof of concept for this immunotherapy approach. Future in vivo experiments will elucidate the actions of this vaccine on addiction mechanisms and facilitate the development of this approach as a therapy to help people overcome nicotine addiction.
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Saravia, Santos Rocio 1988. "Novel insights in nicotine addiction : focus on cognitive function." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/665841.

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Cigarette smoking continues to be leading cause of preventable cause of death worldwide. Cognitive modulation by nicotine seems to be a key factor in nicotine addiction. Several studies indicate that initial nicotine intake has a positive effect on cognition, which may contribute to the development of nicotine dependence. Conversely, when chronic nicotine treatment ceases, cognitive functioning is altered. The orexin and the endocannabinoid system have been reported to play a crucial role in different stages of nicotine addiction and in learning and memory processes. Our results show that orexin receptors influence the pro-cognitive effects of acute nicotine treatment, whereas the endocannabinoid system acting through CB1R modulates the cognitive deficits associated with nicotine withdrawal. In addition, our work reveals an inflammatory process associated with the cognitive deficits of early nicotine abstinence. Given that the presence of cognitive alterations is associated with increased smoking relapse risk, our results identify CB1R and anti-inflammatory drugs as new potential therapeutic strategies for nicotine dependence.
El consumo de cigarrillos es una de las principales causas de muerte prevenible en el mundo. Los efectos de la nicotina sobre la memoria parecen parece ser un factor clave en la adicción a la nicotina. Diversos estudios indican que el consumo inicial de nicotina tiene un efecto positivo sobre la cognición, lo que puede contribuir al desarrollo de la dependencia de la nicotina. Por el contrario, cuando el consumo de nicotina cesa, se altera el funcionamiento cognitivo. Las orexinas y el sistema endocannabinoide desempeñan un papel crucial en las diferentes etapas de la adicción a la nicotina y en los procesos de aprendizaje y memoria. Nuestros resultados demuestran que los receptores de orexina la mejora de memoria inducido por un el tratamiento agudo de nicotina, mientras que el sistema endocannabinoide, actuando a través de los receptores CB1 modula los déficits cognitivos asociados con la abstinencia de nicotina. Además, hemos revelado que un proceso inflamatorio está asociado al desarrollo de los déficits cognitivos de la abstinencia a nicotina. Dado que la presencia de alteraciones cognitivas se asocia con un mayor riesgo de recaída en el hábito de fumar, nuestros resultados identifican a los receptores CB1 y fármacos antiinflamatorios como potenciales nuevas estrategias terapéuticas para la dependencia de la nicotina.
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Kolokotroni, Katerina Zoe. "Nicotine addiction and impulsive behaviour : disentangling the relationship." Thesis, University of Leeds, 2007. http://etheses.whiterose.ac.uk/679/.

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Drug addiction can now be considered a global epidemic with considerable psychological, physical, social and economicc osts. Substantial research remains focused upon furthering our understating of the disorder, for which current treatments are limited in their effectiveness. More recently there has been an increased interest in the multidimensional construct of impulsivity and its association with addiction. Impulsivity is a hallmark feature of drug addiction, with drug users frequently displaying a preference for immediate over delayed gratification (impulsive choice) and a loss of inhibitory control (disinhibition) (Madden et al.,1997). To date, our understanding of the complex association between impulsivity and drug addiction has been hindered by the cross sectional nature of the majority of research conducted. As a result of this it has been unclear whether impulsivity is a risk factor or a consequence of drug abuse. The experiments of this thesis were primarily concerned with exploring the latter of these theories, in the hope of elucidating the role of drug induced impulsivity in the establishment maintenance and relapse of drug dependence. This was achieved by exploring the effects of nicotine in two animal paradigms of impulsivity; the delayed reward paradigm which assessed impulsive choice,and the symmetrically reinforced go/no-go visual discrimination task which measured behavioural disinhibition. A series of preliminary experiments confirmed the suitability of both tasks for exploring the relationship between impulsivity and nicotine dependence. Behavioural disinhibition in the go/no-go task was stable, lacked sensitivity to changes in primary motivation and furthermore appeared not to be dependent on timing mechanisms. Impulsive choice in the delay discounting task was stable and delay sensitive. Whilst decreasing primary motivation was without effect on impulsive choice, increasing motivation for food reward was found to reduce levels of impulsivity. Acutely, nicotine increased both disinhibition (0.5mg/kg,s .c .) and impulsive choice (0.125,0.25,0.5mg/kg,s .c .). The acute effects of nicotine on both components of impulsivity were effectively antagonised by the centrally acting antagonism tecamylamine which alone was without effect in either model. Adopting a longitudinal design, the effects of chronic nicotine administration (3.16mg/kg/day for seven days, osmotic mini pumps), nicotine withdrawal and the residual sensitivity to nicotine following a sustained period of abstinence were then explored. Chronic nicotine administration enhanced disinhibition and impulsive choice, an effect that was greatest at the initial stages of treatment, suggesting that drug tolerance may have developed. Nicotine withdrawal had differential effects on impulsive choice and disinihibition. In the delay discounting task both initial and long-term withdrawal was associated with enhanced sensitivity to delayed reward. This effect, however, was restricted to low "trait" impulsive animals. Conversely, initial withdrawal induced a short-lived rebound increase in inhibitory control, following which a gradual decreasein inhibitory control was observed that reached significance during the second week of withdrawal. Evidence that the effects of nicotine on impulsivity were temporary was shown, with behaviour returning to base line levels three weeks following termination of treatment. Finally, acute nicotine challenges (0.125,0.25,0.5mg/kg, s. c. ) demonstrated that chronic nicotine exposurer endered animals hypersensitive to the effects of nicotine on disinhibition. Overall the present experimental investigations provide evidence to suggest that impulsivity may be a key componenant both the initial and end stages of addiction. Behavioural and pharmacological treatments that target impulsivity may prove to be effective future treatments for the disorder.
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Torres, Oscar Valentin. "Examination of the rewarding effects of nicotine during the adolescent period of development." To access this resource online via ProQuest Dissertations and Theses @ UTEP, 2007. http://0-proquest.umi.com.lib.utep.edu/login?COPT=REJTPTU0YmImSU5UPTAmVkVSPTI=&clientId=2515.

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Cunningham, L. Joseph. "A stop smoking guide for the self-help quitting process." Virtual Press, 1994. http://liblink.bsu.edu/uhtbin/catkey/917044.

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The vast majority of smokers who manage to quit do so without the assistance of a facilitated cessation program. Since the majority of focused anti-smoking efforts are directed at facilitated programs, there is an apparent gap in service of the population at risk. Also, the sharp decline in smoking prevalence indicates a changing demographic dynamic. It is probable that those persons still smoking comprise a different population type than did smokers of a decade ago. A reexamination of major strategies for self-quitting is strongly indicated.The purpose of this thesis was to apply what was known about addictive behavior to a self-guided quitting process. Major variables guiding this effort were learning theory, theory of self-change, empirically demonstrated methods of cessation, and psychosocial effects on lifestyle change.The knowledge gained during the process was incorporated into a menu approach that emphasized personal responsibility for the quitting process and allows for choices that serve to tailor the program to the individual's needs. The end result was a quitters' guide, desktop published and prepared in a small quantity for pilot purposes. This guide was evaluated by persons with particular expertise in addictive behavior, especially smoking cessation. An ammended product was then presented to smokers and/or former smokers for further feedback. A journal of the process that detailed both difficulties and successes was also included.
Fisher Institute for Wellness
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Stennett, Bethany Ann. "Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats." UNF Digital Commons, 2013. http://digitalcommons.unf.edu/etd/465.

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The co-dependence of nicotine and alcohol addiction occurs at high rates, complicates treatment, and is often associated with significant morbidity and mortality. Treatment options of alcohol and tobacco co-dependence are limited. Currently, there are drugs available for nicotine dependence or alcohol dependence. However, there are no therapeutic drugs available on the market for the co-dependence of nicotine and alcohol. Therefore, and important opportunity of new therapeutic options and drug development has presented itself. NT69L, a non-selective neurotensin (NT) agonist, provides a potential novel therapy for nicotine addiction in alcoholics by interacting with the common neurotransmitter circuits supporting the rewarding process for both nicotine and alcohol. Considering the behavioral effects of NT69L in attenuating nicotine self-administration in rats and alcohol consumption in mice, the present study was designed to assess the effects of NT69L as a new drug. NT69L was used in the treatment of nicotine addiction in an animal model of alcoholics and in attempts to attenuate withdrawal signs associated with nicotine and alcohol dependence. Wistar rats pre-exposed to alcohol vapor or air were allowed to self-infuse nicotine (0.03mg/kg/infusion) or saline. When the rats reached a stable level of responding, the effect of pretreatment with NT69L (1mg/kg i.p.) on the reinforcing effect of nicotine was determined. Animals self-infused nicotine at a significantly (p < .05) higher rate compared to saline in both air and alcohol vapor exposed groups. Acute pretreatment with a single injection of NT69L significantly (p < .05) reduced nicotine self-infusion in both the alcohol vapor and the air exposed groups for 5 days post-injection. Additionally, NT69L attenuated the alcohol- and nicotine-induced withdrawal signs associated with the discontinuation of alcohol and nicotine administration. Neurotensin agonist, NT69L, may represent a potential novel therapy to treat the co-addiction of alcohol and nicotine.
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Thompson, Lauren. "Intracellular Signaling Contributions to Behaviors Relevant to Nicotine Addiction." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/253.

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Nicotine is the primary addictive substance in tobacco, and most smokers who quit will relapse within a year. Evidence shows that cigarette craving increases over time, termed “incubation.” The purpose of these studies was to see if protracted abstinence from chronic nicotine increases rat self-administration, an animal model with good face validity for human tobacco use, and if nicotine self-administration during daily exposure/after 8+ days of abstinence is regulated by extracellular signal-regulated kinase (ERK) signaling in the nucleus accumbens (NAc) shell or anterior cingulate cortex (PFC). ERK kinase inhibitor U0126 was infused in the NAc shell or PFC of Long Evans rats immediately prior to daily self-administration sessions and following 8+ days of abstinence. U0126 in the PFC decreased responding for nicotine during daily sessions. Following 8+ days of abstinence, animals showed a robust increase in responding for nicotine, blocked by U0126 in the NAc shell, but not the PFC. Western blots revealed that nicotine treatment decreased levels of a substrate of ERK, ribosomal s6 kinase (RSK), in the NAc shell and increased it in the PFC, which occurred independent of abstinence period. In contrast, levels of RSK were increased in the NAc shell following a nicotine challenge during the abstinence period. In summary, our data show that the ERK signaling pathway plays a vital role in nicotine addiction during daily nicotine exposure and following periods of abstinence.
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De, Preter C. C., Liza J. Hernandez, Seth L. Kirby, R. B. Campbell, E. Beaumont, C. A. Bradley, Matthew I. Palmatier, and Russell W. Brown. "Adolescent Methylphenidate Exposure Alters Nicotine Self-Administration and the Accumbal Firing Response to Nicotine." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/971.

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This study was designed to analyze the effects of adolescent exposure to methylphenidate (MPH; trade name: Ritalin) on nicotine self-administration, the motivation to obtain nicotine, and accumbal neuronal firing rate in female adolescent rats. MPH is the most commonly prescribed medication for Attention Deficit-Hyperactivity Disorder (ADHD) which is diagnosed in 3-5% of adolescents in the United States. However, this disorder is often misdiagnosed, and MPH is often prescribed to individuals not diagnosed with ADHD. Adolescent female Sprague-dawley rats were ip administered 1 mg/kg MPH or saline using a “school day” regimen of five days on, two days off, beginning on postnatal day (P)28 and this regimen was maintained throughout testing. A 1 mg/kg dose of MPH has been shown to result in brain plasma levels equivalent to clinical dosing in humans. Indwelling catheters were implanted in the jugular vein at P35, and one week later on P42, animals began nicotine self-administration. MPH (1 mg/kg) was administered each day approximately 6 h before each self-administration session began, which allows for nearly full plasma clearance of MPH (half-life = 1 h) before self-administration commenced. Rats were reduced to 85% of their free-feeding body weight and sipper tubes were made available to the rats in this paradigm, and responses to licking the tube produced an infusion of nicotine solution (15μg/kg) over a range of fixed ratio (FR) reinforcement schedules followed by a progressive ratio (PR) schedule, a measure of motivation. The schedule of reinforcement during 60 min sessions was increased from an FR5 to FR15 over approximately a three-week period. Results revealed that MPH pre-exposed rats self-administered significantly higher amounts of nicotine as compared to animals treated with saline throughout the FR5 and FR10 schedules. Further, MPH enhanced the motivation to self-administer nicotine on the PR schedule compared to controls, demonstrating an enhanced motivation to obtain nicotine produced by MPH. Finally, animals that had been pre-exposed to MPH and self-administered nicotine demonstrated a lower rate of basal accumbal firing as compared to controls, but a burst firing in response to nicotine that was higher than rats pre-exposed to saline. In conclusion, MPH altered the behavioral and neural response to nicotine in the nucleus accumbens.
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Books on the topic "Nicotine addiction"

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National Institute on Drug Abuse, ed. Nicotine addiction. [Washington, D.C.]: National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 1998.

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National Institute on Drug Abuse., ed. Nicotine addiction. [Washington, D.C.]: National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 1998.

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National Institute on Drug Abuse., ed. Nicotine addiction. [Washington, D.C.]: National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 1998.

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Price, Sean. Nicotine. New York: Chelsea House, 2008.

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Foundation), Symposium on Understanding Nicotine and Tobacco Addiction (2005 Novartis. Understanding nicotine and tobacco addiction. Chichester, UK: John Wiley & Sons, 2006.

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Henningfield, Jack E. Nicotine: An old fashioned addiction. New York: Chelsea House Publishers, 1985.

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Bock, Gregory, and Jamie Goode, eds. Understanding Nicotine and Tobacco Addiction. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470029237.

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Frenk, Hanan, and Reuven Dar. A Critique of Nicotine Addiction. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/b111440.

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Henningfield, Jack E. Nicotine: An old-fashioned addiction. London: Burke Publishing Co., 1985.

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Henningfield, Jack E. Nicotine: An old fashioned addiction. New York: Chelsea House Publishers, 1992.

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Book chapters on the topic "Nicotine addiction"

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Karam-Hage, Maher, Jennifer Minnix, and Paul M. Cinciripini. "Nicotine." In Addiction Medicine, 417–43. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0338-9_19.

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Patterson, Freda, Robert A. Schnoll, and Caryn Lerman. "Nicotine." In Addiction Medicine, 991–1016. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0338-9_49.

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DiFranza, Joseph. "Nicotine Addiction." In Encyclopedia of Cancer, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4081-3.

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DiFranza, Joseph. "Nicotine Addiction." In Encyclopedia of Cancer, 3097–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4081.

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DiFranza, Joseph. "Nicotine Addiction." In Encyclopedia of Cancer, 2518–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4081.

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Froehlich, Stephan J., Carlo A. Lackerbauer, Guenter Rudolph, Jan Rémi, Soheyl Noachtar, Werner J. Heppt, Annette Cryer, et al. "Nicotine Addiction." In Encyclopedia of Molecular Mechanisms of Disease, 1477. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7843.

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Hsia, Stephanie L., Anna K. Mischel, and Arthur L. Brody. "Nicotine." In Absolute Addiction Psychiatry Review, 105–20. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33404-8_7.

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Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick, et al. "Nicotine Dependence and Nicotine Addiction." In Encyclopedia of Behavioral Medicine, 1335. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_101152.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Nicotine/Tobacco Addiction." In Encyclopedia of Psychopharmacology, 887. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3431.

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Rassool, G. Hussein. "Tobacco and Nicotine." In Understanding Addiction Behaviours, 143–56. London: Macmillan Education UK, 2011. http://dx.doi.org/10.1007/978-0-230-34456-3_10.

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Conference papers on the topic "Nicotine addiction"

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Zobena, Aija. "Student Tobacco Use Behaviours: A Qualitative Study of Alternative Tobacco and Nicotine Product Use in Young Adulthood." In 14th International Scientific Conference "Rural Environment. Education. Personality. (REEP)". Latvia University of Life Sciences and Technologies. Faculty of Engineering. Institute of Education and Home Economics, 2021. http://dx.doi.org/10.22616/reep.2021.14.043.

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Non-combustible alternative tobacco products such as tobacco-free nicotine pouches, heated tobacco, and electronic cigarettes (e-cigarettes) marketed as less harmful alternatives to cigarettes as smoking cessation aids are becoming increasingly popular among adolescents and young adults. This age group includes individuals still experimenting with and establishing tobacco use. The aim of the study is to investigate student tobacco use behaviours, particularly novel devices, and alternative products to understand how to decrease tobacco initiation and use among adolescents and young adults. In August 2020, two focus group discussions were organized to obtain information on young people's experience of alternative tobacco and nicotine product use. In each of them, high school students (aged over 18) and students took part. The participants of the focus group discussion were chosen by the “snowball” method. Cessation of smoking and replacing cigarettes with alternative tobacco and nicotine products reduce some of the harmful effects but are not harmless and nicotine addiction remains. By replacing cigarette smoking with the use of tobacco-free nicotine pouches, heated tobacco, or e-cigarettes, one form of nicotine use is being replaced by another. According to the study, young people have no understanding of nicotine addiction and the health risks of using alternative tobacco products. Today's adolescents and young adults often see consumption of tobacco and nicotine products as a mean to construct and project their unique identity.
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Uysal, Mehmet Atilla, Ulgen Sever, and Sacide Pehlivan. "The dopamine receptor D4 VNTR 48bp gene variant in nicotine addiction." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa1486.

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Vergara, Victor M., and Vince D. Calhoun. "Nicotine Addiction Decreases Dynamic Connectivity Frequency In Functional Magnetic Resonance Imaging." In 2020 IEEE Southwest Symposium on Image Analysis and Interpretation (SSIAI). IEEE, 2020. http://dx.doi.org/10.1109/ssiai49293.2020.9094610.

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Al-Wadei, Hussein A., Mohammed H. Al-Wadei, and Hildegard M. Schuller. "Abstract 3231: Chronic nicotine stimulates lung adenocarcinoma in vivo and in vitro via modulation of nicotinic acetylcholine receptor regulated excitatory and inhibitory neurotransmission characteristic of nicotine addiction." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3231.

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White, A. T., P. Williams, V. Anand, J. Benjamin, and S. Kim. "Cigarettes and Straws: Late Positive Potential Modulation in Mental Illness and Nicotine Addiction." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857001.

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Ohar, Jill A., Alireza Sadeghnejad, Deborah A. Meyers, and Eugene R. Bleecker. "CHRNA3/5 SNP RS8034191 Is Associated With Nicotine Addiction That Leads To CAD." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4098.

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Tiunova, S. A., I. I. Logvinova, and L. N. Tsvetikova. "Indicators of lipid peroxidation and antioxidant protection in newborns from mothers with nicotine addiction." In ТЕНДЕНЦИИ РАЗВИТИЯ НАУКИ И ОБРАЗОВАНИЯ. НИЦ «Л-Журнал», 2015. http://dx.doi.org/10.18411/lj2015-11-38-42.

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Sever, Ulgen, Mehmet Atilla Uysal, and Sacide Pehlivan. "Relationship between cigarette (nicotine) addiction and dopamine receptor D2 gene variants (TaqlA and -141C Ins/ Del)." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa1482.

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Batista, Victor de Sousa, Lourival Rodrigues de Sousa Neto, Roberto Ribeiro Faria, Keli Cristina Barbosa dos Reis, and Nailton Monteiro do Nascimento Júnior. "Post-processing of docking results through docking-based comparative intermolecular contacts analysis (dbCICA) of the α4β2 and α7 nicotinic acetylcholine receptors (nAChRs)." In VIII Simpósio de Estrutura Eletrônica e Dinâmica Molecular. Universidade de Brasília, 2020. http://dx.doi.org/10.21826/viiiseedmol2020146.

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The nAChRs are pentameric ligand-gated ionic channels that respond to the endogenous neurotransmitter acetylcholine, with the α4β2 and α7 subtypes being highly expressed in human brain. Those receptors are involved in many neurologic disorders such as Alzheimer’s disease and Schizophrenia, as well as in nicotine addiction. In this context, molecular modelling is a powerful tool for designing novel ligands targeting those receptors. In the present work, we applied dbCICA1 to identify optimal docking conditions for these two receptors. The methodology and results are summarized bellow. Briefly, bioactive compounds acting on each receptor where docked into the crystal structures obtained from PDB (5KXI2 for α4β2 and 5AFH3 for α7) using GOLD4 and the results were post-processed through dbCICA, a genetic algorithm based approach.
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Verde, Audrey R., Jean-Baptiste Berger, Aditya Gupta, Mahshid Farzinfar, Adrien Kaiser, Vicki W. Chanon, Charlotte Boettiger, et al. "UNC-Utah NA-MIC DTI framework: atlas based fiber tract analysis with application to a study of nicotine smoking addiction." In SPIE Medical Imaging, edited by Sebastien Ourselin and David R. Haynor. SPIE, 2013. http://dx.doi.org/10.1117/12.2007093.

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Reports on the topic "Nicotine addiction"

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Newsham, Andrew, Toendepi Shonhe, and Tsitsidzashe Bvute. Commercial Tobacco Production and Climate Change Adaptation in Mazowe, Zimbabwe. Institute of Development Studies (IDS), September 2021. http://dx.doi.org/10.19088/apra.2021.023.

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There has been an increasingly well-documented, rapid rise in tobacco production over the last couple of decades in Mazowe, Zimbabwe, despite growing public health concerns about lung cancer and nicotine’s addictive capacities in the wealthier countries of the West – even affecting the South African market. This has been accompanied by a shift away from its production almost completely on large-scale farms towards predominantly small-scale farms. To date, less consideration has been given to the implications of climate change for tobacco production. Given the hopes that it can make a serious contribution to poverty reduction and food security, it is of increasing importance to understand these implications, to identify the most relevant and/or effective adaptation options and to assess the viability of their successful adoption. This paper presents a fine-grained, qualitative bottom-up analysis of the implications for commercial tobacco production of climate change impacts in Zimbabwe.
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