Orientador: Dionei Ramos / Banca: Moacir Fernandes de Godoy / Banca: Ercy Mara Cipulo Ramos / Resumo: O tabagismo é considerado um dos principais fatores de risco modificáveis de doenças cardiovasculares e suas complicações, dentre as quais doença vascular aterosclerótica, hipertensão, infarto do miocárdio, angina instável e morte súbita. Os efeitos cardiovasculares promovidos pela nicotina ocorrem principalmente, devido ao aumento da atividade simpática, decorrente do estímulo de liberação de catecolaminas, por meio da ativação dos receptores nicotínicos localizados nas terminações nervosas simpáticas pós-ganglionares periféricas e medula adrenal. Além disso, o fumo acarretada uma disfunção autonômica a qual pode ser avaliada por meio da variabilidade da freqüência cardíaca (VFC) que descreve as oscilações dos intervalos entre batimentos consecutivos (intervalos RR) e reflete a atividade do sistema nervoso autônomo (SNA) sobre o nódulo sinusal, sendo uma ferramenta clínica para avaliar e identificar comprometimentos na saúde. Estudos demonstram que o tabagismo crônico leva a ativação simpática e redução da modulação vagal, de forma que essas alterações autonômicas basicamente se expressam por diminuição dos índices de VFC em fumantes. A redução da VFC é considerada uma condição de alta morbidade e mortalidade cardíaca, no entanto, alguns estudos apontam que a cessação do tabagismo pode levar a restauração da função autonômica... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Smoking is considered an important modifiable risk factor for cardiovascular disease and its complications, such as atherosclerosis, hypertension, myocardial infarction, instable angina and sudden death. The cardiovascular effects promoted by nicotine are caused by increased sympathetic activity occurred because of catecholamine release by nicotinic receptors activation at peripheral postganglionic sympathetic nerve endings and adrenal medulla. Moreover, smoking leads to autonomic dysfunction that can be evaluated by heart rate variability (HRV) which describes the oscillations in the interval between consecutive heart beats (RR interval) and reflects the autonomic nervous system (ANS) activity on the sinus node and as a clinical instrument to assess and identify health involvements. Studies have been demonstrated that chronic smoking causes sympathetic activation and reduces vagal modulation and that autonomic alterations basically are showed by decreases of HRV indices in smokers... (Complete abstract click electronic access below) / Mestre

Resumo: Introdução: A nicotina, uma das drogas mais nocivas a saúde, causa, entre outros fatores, morbidade do enxerto ósseo e compromete a cicatrização óssea. Por outro lado, o tratamento com laser em baixa intensidade pode proporcionar efeitos bioestimulantes, aumentando a microcirculação sanguínea da área irradiada e estimulando fibroblastos, promovendo melhores condições de cicatrização. O objetivo do presente estudo foi analisar a influência do laser em baixa intensidade sobre o processo de reparo de enxertos ósseos autógenos em bloco instalados em animais modificados sistemicamente pelos efeitos indesejáveis da nicotina. Materiais e Métodos: Foram utilizados 72 ratos (Wistar) divididos em Grupo A (n=36), subgrupos GI e GII, submetidos à aplicação de nicotina e Grupo B (n=36), subgrupos GIII e GIV, submetidos à aplicação de solução fisiológica. Transcorridos 30 dias das aplicações, todos animais receberam enxerto ósseo autógeno na mandíbula, tendo como área doadora o osso parietal da calvária, sendo que os animais pertencentes aos subgrupos GII e GIV, receberam o tratamento com laser em baixa intensidade na interface enxerto-leito receptor. Os animais de cada grupo foram submetidos à eutanásia aos 7, 14 e 28 dias pós cirurgia de enxerto. Após o processamento laboratorial de rotina foi realizada a análise histomorfométrica, visando analisar qualitativamente e quantitativamente as etapas presentes nesse processo de reparo ósseo. Resultados: A análise histológica revelou que o grupo nicotina apresentou um atraso da atividade osteogênica na interface enxerto-leito receptor, como também menor organização do tecido de granulação em substituição ao coágulo sanguineo. Contudo, a irradiação do tecido com laser em baixa intensidade proporcionou melhor reparo ósseo. Histometricamente, os subgrupos submetidos à irradiação laser... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Background: The nicotine is one of the mostly drugs more harmful to the health cause, among other factors, morbidity of bone graft and compromises bone healing. Furthermore, treatment with low level laser can provide biostimulation effects, increasing the blood microcirculation in the irradiated area and stimulating fibroblasts promoting better healing. The aim of this study was to evaluate the influence of low level laser therapy on the healing process of autogenous bone grafts installed in block in systemic modificated animals by undesirable effects of nicotine. Methods: Were used 72 rats (Wistar) divided into Group A (n = 36) subgroups GI and GII, submitted to the application of nicotine and Group B (n = 36) subgroups GIII and GIV, submitted to the application of saline solution. After 30 days of applications, all animals received autogenous bone block graft stabilized on mandible, with the parietal bone donor area of the skull, and the animals belonging to subgroups GII and GIV received treatment with low level laser in the bed-graft interface. The animals in each group were euthanized at 7, 14 and 28 days after bone graft surgery. After routine processing was performed histomorphometric analysis in order to analyze qualitatively and quantitatively the timing sequence of bone repair. Results: The histological analysis revealed that the nicotine group showed a delay of osteogenic activity in the bed-graft interface, as well as decreased organization of granulation tissue replacing the blood clot. However, the low level laser irradiation showed better bone healing. Histometrically, the laser subgroups (GII and GIV) demonstrated greater bone formation compared with the respective subgroups (GI and GIII), with significantly statistically results (P˂0) at 14 days (GI 14,27% ± 2,22% versus GII 24,37% ± 11,93% and GIII 24,94% ± 13,06% versus ...(Complete abstract click electronic access below) / Orientador: Álvaro Francisco Bosco / Coorientador: Valdir Gouveia Garcia / Banca: Juliano Milanezi de Almeida / Banca: Leticia Helena Theodoro / Mestre

Conselho Nacional de Desenvolvimento Científico e Tecnológico / Uma questão particularmente relevante é o fato de exposições precoces a drogas de abuso durante o desenvolvimento potencialmente aumentarem a susceptibilidade a estas drogas posteriormente durante o desenvolvimento. No presente estudo utilizando estudos comportamentais e eletrofisiológicos, investigamos efeitos tardios da exposição de camundongos à fumaça de cigarro, à nicotina e ao etanol durante o período que corresponde à gestação em humanos. Para tal, esta tese foi dividida em 2 estudos. No Estudo 1, submetemos camundongos durante o período que corresponde à gestação de humanos à fumaça de cigarro e/ou etanol visando investigar se a estas drogas de abuso, separadamente ou quando combinadas, programam maior susceptibilidade aos efeitos da nicotina durante a adolescência (PN30) ou idade adulta (PN90). Para avaliar a susceptibilidade, utilizamos 3 testes: campo aberto (CA), preferencia pela nicotina (PPN) e preferencia condicionada por lugar (CPP). No Estudo 2, os animais foram expostos a nicotina durante o período gestacional e, no período que corresponde à infância (PN9 a PN20), fatias de cérebro contendo o núcleo tegumental laterodorsal (LDT) foram expostas a etanol. Este núcleo foi escolhido uma vez que estudos recentes indicam sua participação em mecanismos de toxicodependência. Foram realizados registros eletrofisiológicos de uma única célula. No Estudo 1, identificamos maior sensibilidade para os efeitos da reexposição à nicotina na adolescência quando comparada com a idade adulta . Em animais testados no CA durante a adolescência, a nicotina foi capaz de causar aumento da atividade locomotora nos animais controle, previamente expostos à fumaça de cigarro e ao etanol. Contudo, em animais expostos à fumaça combinada com etanol, não houve aumento da locomoção. Na idade adulta, a nicotina causou um aumento da atividade locomotora no CA somente nos animais expostos à fumaça de cigarro. Quanto ao CPP, a exposição prévia à fumaça de cigarro e ao etanol causaram aumento da resposta condicionada à nicotina em fêmeas adolescentes. Nos animais previamente expostos à combinação entre fumaça de cigarro e etanol, a resposta condicionada à nicotina não atingiu significância estatística. Não houve alterações na idade adulta. A exposição a fumaça de cigarro e/ou etanol não afetou a PPN. No Estudo 2, os dados eletrofisiológicos mostraram que a exposição pré-natal à nicotina foi capaz de alterar as correntes de despolarização basais e o potencial de repouso de células do LDT A nicotina também foi capaz de alterar as respostas deste núcleo ao etanol reduzindo as correntes de despolarização e aumentando, embora que não de forma significativa, as correntes inibitórias. De acordo com estes dados, injurias causadas pela exposição à fumaça do cigarro, à nicotina isoladamente, e ao etanol durante o desenvolvimento são capazes de perdurar por um logo tempo na vida do individuo, alterando as respostas a comportamentais e celulares a uma exposição tardia à nicotina e ao etanol. / Particularly relevant is the fact that early exposure to drugs of abuse during development potentially increases drug susceptibility later during development. In the present study we used mice models to investigate postnatal behavioral and electrophysiological effects of exposure to cigarette smoke, nicotine and ethanol during the period that corresponds to pregnancy in humans. To this end, this thesis was divided into two studies. In Study 1, we submitted mice to cigarette smoke and / or ethanol in order during the period that corresponds to human pregnancy to investigate whether these drugs of abuse, alone or when combined, programs increased susceptibility to the effects of nicotine during adolescence (PN30) or adulthood (PN90). To evaluate susceptibility, we use three tests: open field (OF), preference for nicotine (PFN) and conditioned place preference (CPP). In Study 2, the animals were exposed to nicotine during pregnancy and, in the period corresponding to childhood (PN9 to PN20), brain slices containing the laterodorsal tegmental nucleus (LDT) were exposed to ethanol. This nucleus was chosen based on recent studies that indicate that it participates in mechanisms of addiction. Whole cell patch clamp recordings were performed. In Study 1, a higher sensitivity to the effects of nicotine exposure was identified during adolescence when compared to adulthood. In animals tested in the OF during adolescence, nicotine was able to cause an increase in locomotor activity in controls, in mice previously exposed to cigarette smoke, and in those exposed to ethanol. However, nicotine failed to increase locomotion in mice previously exposed to smoke combined with ethanol. In adulthood, nicotine caused an increase in OF locomotor activity only in animals exposed to cigarette smoke. In the CPP, previous exposure to cigarette smoke, and to ethanol caused an increase of the conditioned response to nicotine in adolescent females. In animals previously exposed to the combined cigarette smoke and ethanol, the conditioned response to nicotine did not reach statistical significance. There were no changes in adult mice. Exposure to cigarette smoke and / or ethanol did not affect the PFN. In Study 2, electrophysiological data have shown that prenatal exposure to nicotine alters the pattern of basal and depolarization of the resting potential of cells LDT. Nicotine was also able to change the answers this core ethanol reducing and increasing depolarization currents, although not significantly inhibitory currents. According to these data, injuries caused by exposure to cigarette smoke, nicotine alone, and ethanol during development persist during postnatal development, changing the behavioral and cellular responses to a late exposure to nicotine and ethanol.

This thesis deals with "Smoking of senior Citizens". Smoking of tobacco is the most significant reason of illnesses and early death in the Czech Republic. Reduction of smoking is a basic condition for decrease of deaths caused by tumour and cardiac diseases.The goal of the thesis is to monitor prevalence of smoking in senior citizens and detect their awareness of smoking. 206 respondents at the age of sixty and above paricipated in this research. 50 % of these people vrote that they had never snoked. 20 % of informants were active smokers, at the time of this survey, and 55 % of senior citizens wrote that they considered nicotine addiction to be a disease.The author tries to verify the hypothesis concerning smoking of senior citizens who suffer from chronic disease. 44 % of the respondents, who were active smokers at the time of the survey, suffered from chronic disease. The researcher uses the next hypothesis because she wants to confirm the fact that senior citizens have a positive attitude to prohibition of smoking in the restaurants and in public areas. The research verified this hypothesis - 72 % of the informants had a positive attitude to prohibition of smoking in public.

A hipertensão arterial é um problema de saúde pública no Brasil, pois aproximadamente 20 % da população adulta desenvolve hipertensão essencial, cujas causas ainda não são conhecidas. No entanto, sua gênese pode estar relacionada com disfunção nas áreas do sistema nervoso central (SNC) que regulam o sistema cardiovascular. O núcleo do trato solitário (NTS) e o bulbo ventrolateral são áreas importantes no controle neural da pressão arterial. Os receptores de adenosina A2a (rA2a) são encontrados em todo o SNC e estão relacionados com estudos terapêuticos de diversas doenças. No NTS a estimulação dos rA2a provoca ajustes pontuais em outros sistemas de neurotransmissão, além de diminuir a pressão arterial. A nicotina é uma molécula com uma vasta faixa de efeitos modulatórios em nosso organismo. Entre esses efeitos se destacam a capacidade de interagir com diversos sistemas de neurotransmissão nas áreas do bulbo relacionadas com a regulação da pressão arterial e de antecipar e/ou intensificar o desenvolvimento da hipertensão em sujeitos com pré-disposição genética. Desta forma, o objetivo do presente trabalho é avaliar o efeito modulatório da nicotina sobre o rA2a em cultura mista de neurônios e células gliais da porção dorso-medial do bulbo de ratos geneticamente hipertenso (SHR) e normotensos (WKY). Para isso, utilizaram-se técnicas como a de PCR em tempo real, Western Blotting e análise de ligação do receptor. Nossos resultados demonstraram que: 1) em condição basal células de ratos normotensos apresentam maior ligação do rA2a do que células de ratos hipertensos; 2) tratamento com nicotina resultou na diminuição da ligação do receptor em ambas as cepas, com um efeito de maior magnitude em células de ratos WKY; 3) nas duas linhagens o tratamento com nicotina alterou os níveis protéicos do rA2a, assim como o RNAm do receptor; 4) a linhagem e o tratamento separadamente, como a interação entre ambos influenciaram na expressão do RNAm , níveis protéicos e ligação do rA2a nas células dos ratos WKY e SHR. Por fim, os resultados apresentados aqui indicam que o rA2a em células de ratos hipertensos tem sua função deprimida em comparação com as células de ratos normotensos; e que a nicotina foi capaz de modular o funcionamento do rA2a, o qual pode influenciar no controle da pressão arterial. Esses dados são bastante interessantes, pois abrem novas perspectivas de análise dos mecanismos intracelulares envolvidos na modulação dos rA2a pela nicotina, assim como a importância desse sistema no desenvolvimento da hipertensão / Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated with morbidity and mortality and the cost to the society, it became an important public health challenge in Brazil. The mechanisms involved in development of hypertension still remain unclear However, hypertension can result from neuronal network imbalance in areas of the central nervous system that control blood pressure. The nucleus tractus solitarius (NTS) plays an important role in cardiovascular control. Within the NTS there are several neurotransmitters and neuromodulatory substances, such as adenosine, which acts on purinoreceptors A2a (A2ar). The A2ar modulates neurotransmission in the NTS and its activation may induce decrease in blood pressure by different mechanisms. Nicotine is a molecule that cross the blood-brain barrier and acts in several areas of central nervous system including the NTS. In this nucleus, nicotine is able to interact with some neurotransmitter systems and contributes for the development of hypertension in subjects with genetic predisposition to this disease. The goal of this study was to analyze the modulatory effects of nicotine on A2ar in cultured neurons and glial cells from medulla oblongata of normotensive (WKY) and spontaneously hypertensive rats (SHR). By means of real time PCR, Western Blotting and binding receptor assay. We have demonstrated that in basal condition cells of WKY presents increased binding of A2ar than the cells of SHR. Nicotine treatment induced a decrease in the binding of A2ar in both strains, however, this response was more pronounced in cells of WKY than SHR. Changes in mRNA and protein levels of A2ar was also observed in response to nicotine treatment. The strains and treatment separately, as well as the interaction between them influenced mRNA expression, protein level and binding of A2ar in NTS cells of WKY and SHR rats. Finally, these results show for the first time changes in A2ar mRNA expression, protein level and binding in cells from the medulla oblongata of WKY and SHR rats, as well as, the nicotine modulation upon this system, which might influence cardiovascular control. These data open up new approaches for the study of intracellular mechanisms involved in the modulation of adenosine A2a receptor by nicotine, as well as the importance of this interaction in the development of hypertension.

Philosophiae Doctor - PhD / Lung cancer is the most common fatal cancer in terms of both incidence and mortality in the world. The most important cause of lung cancer is exposure to tobacco smoke through active or passive smoking. Nicotine which is a major component of tobacco could be assumed to be a tumour promoter since it had been indicated to stimulate tumour growth. Over expression of Bcl-2 in human lung cancer cells blocked the induction pathways (type I and II) of apoptosis. The increase in Bcl-2 in patients with lung cancer had also been linked to nicotine. In recent years nicotine replacement therapy has become a therapeutic method to treat smoker’s withdrawal symptoms and to advise cancer patients to stop smoking because, numerous cancer patients continue to smoke after their diagnosis. Non small cell lung carcinomas constitutes for approximately 80% of lung cancer cases. However, even with the development and improvement in conventional treatments of surgery, radiation and chemotherapy, the 5 year survival rate for these patients remains less than 15%. Chemoprevention, an approach to control cancer, is the use of specific natural or synthetic substances with the objective of delaying, reversing, suppressing or preventing carcinogenic progression to invasive cancer. A promising tool for chemoprevention against lung cancer could be prostaglandin A2 (PGA2), since it had been shown to have inhibitory effects on various cancer cell growth. The search for more effective agents, or combination therapies that could induce apoptosis in lung cancer are currently under investigation as a therapeutic target for the treatment of lung cancer. In order to elucidate the effect of nicotine and PGA2 on lung cancer cell proliferation in this study, an over view of the following was given;the cell cycle, tubulin, nucleoli, apoptosis, lung cancer, the etiology of cancer with reference to tobacco smoke and nicotine, the nutritional influence on carcinogenesis with reference to essential fatty acids and prostaglandins and chemoprevention.The supplements nicotine and PGA2 were administered to the NCI-H157 lung cancer cell line at the concentrations of 1 mM, 1 μM and 1 nM for nicotine and 5, 10 and 20 μg/ml PGA2. The effect of combinations of nicotine and PGA2 on the proliferation and survival was also tested. 5 μg/ml PGA2 was added to 1 mM, 1 μM and 1 nM nicotine respectively. This was also done for 10 and 20 μg/ml PGA2.These concentrations were administered to the cell culture and exposed for three different time exposures, namely 24, 48 and 72 hours. The objectives were: 1) To determine the effect of nicotine and PGA2 and combinations thereof on the growth(proliferation) of the NCI-H157 cells, where early results indicative of apoptosis lead to the investigation of the influence of nicotine and PGA2 on apoptosis. The effect of nicotine and PGA2 and their combinations on the morphology of interphase and dividing cells, as well as on the morphology of the dying cells were compared and quantified. 2) To study the effects of nicotine and PGA2 and their combinations on the nucleolar organizer region using silver stain. 3) To study the effects of nicotine and PGA2 or combinations thereof on the cytoskeleton (α-tubulin) of the cancer cells with aid of indirect immunofluorescence and to identify apoptotic cells using Hoechst 33342. 4) To determine the effect of nicotine and PGA2 and their combinations on cell cycle progression and apoptosis induction in the transformed cells using flow cytometry (DNA propidium iodide stain, Annexin V and caspase-3).In order to verify the effects of nicotine and PGA2 and their combinations on protein synthesis, SDS-PAGE and immunoblotting was employed.This study indicated the anti-apoptotic effects of nicotine. It maintained and stimulated cell proliferation of the NCI-H157 cell line. PGA2 demonstrated that it has a pro-apoptotic effect. The concentrations of 10 and 20 μg/ml PGA2 decreased cell proliferation and demonstrated its pro-apoptotic effects more effectively than 5 μg/ml PGA2. The combination of 10 and 20 μg/ml PGA2 and nicotine (1 mM, 1 μM and 1 nM) also showed a more pronounced induction of apoptosis than 5 μg/ml PGA2 and nicotine (1 mM, 1 μM and 1 nM). PGA2 therefore demonstrated that it blocked the mitogenic and anti-apoptotic effects of nicotine. With its pro-apoptotic effects, PGA2 could therefore be assumed to be a chemopreventive agent. However,it was evident that apoptotic induction was stimulated via both a dependent and an independent caspase-3 pathway and therefore further investigation is needed to indicate which pathway was activated. This study identified PGA2 as a chemopreventive agent for in vitro conditions; however, further studies are also needed to investigate the effect of in vivo conditions.

No description available.

M.A. / Literature indicates that childhood ADHD has received considerable attention and recognition in today’s society and is effectively represented in the DSM. In comparison, there is still much controversy surrounding ADHD in adults (aADHD), despite the fact that almost 50 to 70% of people diagnosed with childhood ADHD continue to manifest symptoms in adulthood. Research indicates that aADHD manifests differently to childhood ADHD, in that the core symptom is inattention and not hyperactivity. Research also indicates that there is a high comorbidity between aADHD and substance dependence, including nicotine dependence. It is hypothesized that these individuals present with hypodopamine, and nicotine acts on a number of neurotransmitter pathways, including the dopaminergic and acetylcholinergic pathways, effectively stimulating the release of dopamine. Whilst there is considerable literature on nicotine and ADHD, there is a complete lack of literature on the relationship between aADHD and Hookah Pipe smoking. This study aimed to rectify this situation. The present study was conducted with two major purposes in mind: (1) to investigate the relationship between Hookah Pipe smoking and its effects on attention and concentration in young adults with Attention Deficit/Hyperactivity Disorder (ADHD) symptomatology, and (2) to demonstrate whether Hookah has a greater effect than cigarettes (as Hookah reportedly has higher concentrations of nicotine than cigarettes). A total sample of 39 participants (14 males, 35 females) aged 18 to 26 years was recruited and divided into the following six groups using the ASRS, the Burke-Austin Self-Report ADHD Questionnaire and a substance abuse questionnaire as screening tools: ADHD (Hookah), ADHD (Nicotine), ADHD (Non-Smoking), Non-ADHD (Hookah), Non-ADHD (Nicotine) and Non-ADHD (Non-Smoking). Furthermore, a quasi-experimental research design was used, whereby the Cambridge Neuropsychological Test Automated Battery (CANTAB) ADHD Battery was administered across three test conditions, with a seven minute intervention between the pre- and post-intervention, and a 90 minute waiting period between the immediate and intermediate post-intervention, so as to test the effects of the nicotine as it neared its elimination half-life of two hours.

Magister Scientiae (Medical Bioscience) - MSc(MBS) / Several studies conducted in laboratories at the University of the Western Cape has demonstrated an interference with the parenchymal lung tissue of the offspring when exposed to nicotine (smoking cigarettes and/or Nicotine Replacement Therapy [NRT]), maternally i.e. during gestation and lactation. This in turn, decreases the amount of air sacs (alveolar number) resulting in a reduced surface area available for efficient gas exchange in the offspring. Since the foetus and offspring are only exposed to nicotine during gestation and lactation, emphysema- like lesions appear to develop after nicotine withdrawal in the foetus. It has been proposed that during lung development in utero, a change in the "program" that controls the maintenance of lung integrity will occur in the long term due to the initial maternal nicotine exposure. Therefore, animals that were exposed to maternal nicotine resemble lungs that have undergone rapid, premature aging caused by cellular senescence. Furthermore, energy metabolism and structural changes in the glycolytic pathways appear irreversibly slower compared to animals that were not exposed to nicotine via the mother during gestation and lactation, resulting in a reduction in the anti-oxidant capacity of lung development. Previous studies have also shown that strong anti-oxidants supplemented by smoking mothers during gestation and lactation could possibly resist change in the "program" which controls lung development and integrity of the offspring in the long term. Lycopene – as a strong anti-oxidant supplementation have shown to decrease the alveolar volume and increase the alveolar surface area for better gas exchange after the offspring has been exposed to maternal nicotine. In this study I have treated pregnant wistar rats with nicotine, tomato juice (containing lycopene among other phytonutrients), and a combination of nicotine and tomato juice during gestation, to determine various changes in the lung structure and signs of premature aging in the lungs of the offspring. I have also performed various staining techniques such as H&E, connective tissue and β- galactosidase staining which indicated whether maternal nicotine exposure indeed induced premature cellular senescence in the lungs of the offspring. / National Research Foundation

Investigations into the cognitive effects of tobacco smoking have generally focused on nicotine and its effect on nicotinic acetylcholine receptors (nAChRs) in the brain. However, it is now known that chronic smokers exhibit robust inhibition of the monoamine oxidase (MAO) enzyme through the actions of non-nicotine components in tobacco smoke. Therefore, the primary aim of this thesis is to elucidate the effects of nicotine and MAO-inhibition on electroencephalographic (EEG) and event-related potential (ERP) measures of cognition. 24 healthy nonsmoking males were administered 75 mg of moclobemide, and chewed 6 mg nicotine gum, in order to simulate the effects of acute smoking. Four experimental conditions included placebo, nicotine, moclobemide, and a combination of nicotine and moclobemide. Early auditory ERPs were used as measures of cognition, such as the auditory P50 sensory gating paired-stimulus paradigm, the acoustic-change-elicited mismatch-negativity (MMN), the novel sound-elicited P3a, and the target sound-elicited P3b. Three minutes of eyes closed EEG were also recorded. Because these ERPs are often identified as biomarkers for schizophrenia, drug effects were also measured after individuals were stratified for low-baseline amplitude of each ERP measure, as a laboratory model of cognitive deficits in schizophrenia. Overall results showed a synergistic improvement in sensory gating via nicotine combined with moclobemide, accompanied by a reduction in theta band power. Nicotine in the absence of moclobemide increased P3b amplitude, accompanied by an increase in alpha2 band power. Moclobemide in the absence of nicotine increased P3a amplitude, accompanied by a decrease in beta2 power. Stratifying participants by placebo amplitude revealed both nicotine and moclobemide exhibited an inverted-U pattern of effect, i.e. showing greater amplitude increases in individuals with the lowest baseline amplitudes. Overall, this thesis demonstrates how these two components of tobacco smoke affect different facets of auditory processing in different ways, with synergistic effects in some paradigms but antagonizing effects in others. Therefore, chronic smokers and schizophrenia patients who seek transient cognitive improvement through smoking may actually experience cognitive detriments overall, possibly contributing to withdrawal symptoms and/or an exacerbation of already-present psychiatric symptoms.