ADHD is one of the most common childhood psychiatric disorders affecting 3- 5% of all children. Between 50 and 80% of those diagnosed with ADHD in childhood will show symptoms that persist into adolescence and adulthood. ADHD is characterized by developmentally excessive activity, impulsivity, inattention, and disorganized, off-task behaviors. A high propensity for risk taking is seen in ADHD and is related to negative outcomes such as job failure, accidents and injuries, and substance use. In an attempt to better understand the behavioral and cognitive deficits associated with ADHD, several neuropsychological models have been proposed. We suggest that those models may be used to learn about risk taking propensity in ADHD. Individuals with ADHD smoke cigarettes at twice the rate of individuals who do not have this diagnosis, and they have greater difficulty quitting. And smokers score higher on a behavioral task of risk taking propensity than non-smokers. The strong association between ADHD and cigarette smoking and the known effects of nicotine on cognition has lead to interest in the role of cholinergic function in ADHD cognitive deficits. Previous work demonstrates that acute nicotine improves behavioral inhibition, working memory, and recognition memory in ADHD. This study examined the acute effects of nicotine on risk taking in non-smoking young adults with ADHD-Combined Type and healthy controls. This single-dose, acute, double blind study assessed the effects of transdermal nicotine and placebo on 26 non-smoking young adults (15 healthy controls and 11 ADHD-C). Participants received acute nicotine (7 mg patch for 45 minutes) and placebo on separate days. The Balloon Analogue Risk Task (BART) was used to assess risk taking propensity. Behavioral ratings were completed daily by each subject and by the blinded investigator. Vital sign data were collected at 30 minute intervals throughout each study day. There were no group differences or interaction of drug and group between the ADHD and control group on risk taking propensity. However, using a median split to identify subjects as either high or low in baseline risk taking there was a significant (p<.05) Drug by Group interaction with nicotine reducing risk taking in high risk taking subjects and increasing risk taking in the low risk taking subjects. These findings are consistent with a large body of research demonstrating ratedependent effects of nicotine on behavior, cognition and mood. Nicotine appears to modulate risk-taking in both high and low risk-taking subjects consistent with cholinergic modulation of behavioral decision making.

Kynurenine (KYN) is the first stable metabolite of the kynurenine pathway, the major route of tryptophan. (TRP) metabolIsm. In the liver, cortisol-inducible tIyptophan-2,3-dioxygenase (TDO) is the first enzyme and rate limiting step. In extrahepatic tissues, it is superceded by indoleamine-2,3-dioxygenase (IDO), an enzyme with a wider substrate specificity. Earlier work in this research group has found substantial elevations in plasma KYN in fasting Tourette's Syndrome (TS) patients with normal TRP and neopterin. The aim of our initial pilot study was to confirm this increase in KYN in fasting human TS patients compared with normal controls, and to see how changes in diet :ay influence certain kynurenine pathway variables. However, we failed to detect a change in plasma KYN, TRP, kynurenic acid (KYNA), neopterin or cortisol between the fasting TS and control groups. Moreover, none of the variables was affected by dietary status, and thus candidates selected for the larger cross-sectional study were permitted to eat and drink freely on the day that blood samples were submitted, but were requested to avoid products containing caffeine, aspirin or nicotine. In the cross-sectional study, TS patients exhibited significantly higher plasma KYN concentrations than controls, although the magnitude of the change was much smaller than originally found. This may be due to differences in detection procedure and the seasonal fluctuation of some biochemical variables, notably cortisol. The generalised increase in neopterin in the TS subject group, suggests a difference in the activity of cytokine-inducible IDO as a likely source for this elevated KYN. Other kynurenine pathway metabolites, specifIcally TRP, 3-hydroxykynurenine (HKY), 3-hydroxyanthranilic acid (HAA) and KYNA were unchanged. In view of recent speculation of the potential therapeutic effects of nicotine in TS, the lower KYN concentrations observed in TS smokers, compared with non-smoking TS patients, was another interesting finding. Tic-like movements, such as head-shakes (HS), which occur in rodents both spontaneously and following diverse drug treatments, closely resemble tic behaviours in humans. The animal tic model was used to examine what effects nicotine may have on shaking behaviours and on selected TRP metabolites. Acute systemic administration of nicotine to mice, produced a dose-dependent reduction in HS frequency (induced by the 5-HT2A/2C agonist DOl), which appeared to be mediated via central nicotinic cholinergic receptors, since mecamylamine pretreatment abolished this effect. Conversely, twice daily subcutaneous injections of nicotine for 7 days, led to an increase in spontaneous and DOI-induced HS. Chronic nicotine also caused a significant elevation m plasma and whole brain KYN concentrations, but plasma TRP, HKY, HAA and KYNA were unaltered. In addition, no change in brain 5-HT or 5-HIAA concentrations or 5-HT turnover, was found. Despite contrasting results from human and animal studIes, a role for nicotine in the mediation of tic-like movements is indicated. The relevance of the kynurenine pathway to TS and the potential role played by nicotine in modifying tic-like behaviours is discussed.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Thesis (BA(Hons) (Psychology)) - Faculty of Life and Social Sciences, Swinburne University of Technology, 2006. / "October 2006". Submitted as a requirement for the degree Bachelor of Arts in Psychology with Honours, [Faculty of Life and Social Sciences], Swinburne University of Technology - 2006. Typescript.

Inaug.-Diss.--Marburg. / Vita. Includes bibliographical references.

<p>In the 20th century, where tobacco smoking continues to be the leading preventable cause of death, an alarming number of people continue to smoke, despite awareness of the implications of exposure for themselves and those around them. Campaigns for the promotion of effective tobacco legislation and awareness are continuously being confronted by the tobacco industry's reluctance to put the health of their consumers before company profits, leading to a ripple effect of misinformation, serious health risks and economic implications, at least for the consumers. Pregnant women are especially a concern, because exposure to tobacco smoke affects not only the smoking mother but has serious implications for the health of her unborn child. Therefore, the aim of this study was to investigate the effect of maternal exposure to nicotine during all the phases of lung development, or from the onset of the phase of rapid alveolarisation and, whether copper supplementation will prevent the adverse effects of maternal nicotine exposure, on lung development in the offspring.</p>

<p>In the 20th century, where tobacco smoking continues to be the leading preventable cause of death, an alarming number of people continue to smoke, despite awareness of the implications of exposure for themselves and those around them. Campaigns for the promotion of effective tobacco legislation and awareness are continuously being confronted by the tobacco industry's reluctance to put the health of their consumers before company profits, leading to a ripple effect of misinformation, serious health risks and economic implications, at least for the consumers. Pregnant women are especially a concern, because exposure to tobacco smoke affects not only the smoking mother but has serious implications for the health of her unborn child. Therefore, the aim of this study was to investigate the effect of maternal exposure to nicotine during all the phases of lung development, or from the onset of the phase of rapid alveolarisation and, whether copper supplementation will prevent the adverse effects of maternal nicotine exposure, on lung development in the offspring.</p>

Thesis (M.A.)--University of Texas at El Paso, 2007. / Title from title screen. Vita. CD-ROM. Includes bibliographical references. Also available online.

Thesis (Ph.D.)--Indiana University, 2009. / Title from screen (viewed on September 30, 2009). Department of Medical Neuroscience, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): William J. McBride, R. Andrew Chambers, James M. Murphy, Zachary A. Rodd. Includes vita. Includes bibliographical references (leaves 131-143).

Philosophiae Doctor - PhD / In the 20th century, where tobacco smoking continues to be the leading preventable cause of death, an alarming number of people continue to smoke, despite awareness of the implications of exposure for themselves and those around them. Campaigns for the promotion of effective tobacco legislation and awareness are continuously being confronted by the tobacco industry's reluctance to put the health of their consumers before company profits, leading to a ripple effect of misinformation, serious health risks and economic implications, at least for the consumers. Pregnant women are especially a concern, because exposure to tobacco smoke affects not only the smoking mother but has serious implications for the health of her unborn child. Therefore, the aim of this study was to investigate the effect of maternal exposure to nicotine during all the phases of lung development, or from the onset of the phase of rapid alveolarisation and, whether copper supplementation will prevent the adverse effects of maternal nicotine exposure, on lung development in the offspring. / South Africa