To see the other types of publications on this topic, follow the link: Nicotine.
Dissertations / Theses on the topic 'Nicotine'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'Nicotine.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Harrington, Lauriane. "The role of β4-containing nicotinic acetylcholine receptors in nicotine addiction". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066328/document.
Full textAbstract:
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<br>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
2
Munhoz, Egberto [UNESP]. "Administração subcrônica de nicotina modifica as respostas neuroendócrina e neuroquímica induzidas pelo teste de natação forçada." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/104039.
Full textAbstract:
Made available in DSpace on 2014-06-11T19:32:56Z (GMT). No. of bitstreams: 0
Previous issue date: 2010-12-13Bitstream added on 2014-06-13T18:44:37Z : No. of bitstreams: 1
munhoz_e_dr_arafo.pdf: 3085541 bytes, checksum: f014aca5c4e34e1bd024219270c2acaf (MD5)<br>Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)<br>O estresse, atualmente, é considerado um fator importante na fisiopatologia de muitos distúrbios psiquiátricos. Embora os efeitos do estresse agudo possam ser contrabalanceados por respostas adaptativas, o estresse intenso, repetido ou prolongado pode eliciar alterações neuronais duradouras que constituirão as bases de doenças psiquiátricas, como a depressão. Levantamentos epidemiológicos também mostram elevada prevalência de tabagistas entre pacientes com depressão maior. Estas altas taxas de comorbidade sugerem uma provável relação causal: pacientes com depressão proeminente procurariam a nicotina para alívio dos sintomas. Assim, este trabalho investigou as alterações neuroquímicas e neuroendócrinas mediadas pela nicotina na resposta de adaptação ao estresse, utilizando-se, para tanto, o teste modificado da natação forçada (TNF). Para tanto, ratos Wistar machos foram submetidos ao TNF (30 cm de água, 24 ± 1ºC) por 15 min e tratados (1, 19 e 23h) com nicotina (NIC: 0,5 mg/kg, sc), imipramina (IMI: 15 mg/kg, ip) ou salina (SAL). Uma hora após a última injeção, os animais foram reexpostos (5 min) à mesma cuba. Imediatamente após o teste, os animais foram sacrificados; o hipocampo dorsal (HD) e ventral (HV), hipotálamo (HT) e os núcleos dorsal (DR) e mediano (MR) da rafe foram coletados por punch para quantificação de 5-HT, 5-HIAA e NA por HPLC e o sangue, para quantificação da corticosterona plasmática por radioimunoensaio. O hipocampo total também foi utilizado para avaliar a expressão do receptor serotoninérgico 5-HT1A e do glicorreceptor (GR) por western blot. Ainda, avaliou-se o efeito da prazosina nas alterações neuroquímicas induzidas pelo TNF. O tratamento subcrônico com NIC e IMI reduziu em 39% e 50%, respectivamente, o parâmetro de imobilidade e aumentou em 52% e 66%, respectivamente, as contagens de escalada, em relação ao grupo...<br>Stress is considered a key component in the pathophysiology of several psychiatric diseases. Although the effects of acute stress can be counterbalanced by adaptative responses, intense, repeated or prolonged stress can elicit long lasting neuronal alterations that are related to the occurrence of psychiatric disorders, such as depression. Epidemiological studies have also identified a high prevalence of smokers among depressive patients. These observations suggest a causal relationship: smoking is a self-medication effort to alleviate some symptoms of depression by nicotine. Then, this study investigated nicotine mediatedneurochemical and neuroendocrine alterations in the adaptation response to stress. The modified forced swmming test (FST), a protocol originally employed for screnning new antidepressant drugs, was employed. Male Wistar rats were placed individually into a container (30-cm of water, 24±1ºC, 15 min - pretest). Then animals received nicotine (0.5 mg/kg, s.c.), imipramine (15 mg/kg, i.p.) or saline injections at 1, 19 and 23h after the pretest. One hour after the injections, animals were placed in the same container for 5 min. Immediately after, the animals were sacrificed; dorsal (DH) and ventral (VH) hippocampus, hypothalamus (HT) and dorsal (DR) and median (MR) raphe nuclei were collected by punch for measurement of 5-HT, 5-HIAA and NA by HPLC (expressed in ng/mg tissue). Blood samples were collected for determination of plasma corticosterone levels by radioimmunoassay. The whole hippocampus was also used to evaluate the expression of the 5-HT1A serotoninergic receptor and glucocorticoid receptor by western blot. The effects of prazosin in TNF induced-neurochemical alterations was also evaluated. Nicotine and imipramine decreased in 39% and 50%, respectively, the immobility behavior and increased in 52% and 66%, respectively, the climbing scores, in relation to saline... (Complete abstract click electronic access below)
3
Drasdo, Alison L. "Studies of brain nicotinic acetylchlorine receptors : with respect to nicotine dependence." Thesis, University of Bath, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332792.
Full text
4
James, John Randolph. "Evidence That Nicotine Can Acutely Desensitize Central Nicotinic Cholinergic Receptors In Vivo." VCU Scholars Compass, 1992. http://scholarscompass.vcu.edu/etd/3935.
Full textAbstract:
Current concepts concerning nicotine's central nervous system (CNS) mechanism(s) of action suggest that this drug is producing its effects via an interaction at nicotiniccholinergic receptors (nAChRs) which open a membrane cation channel. Following initial opening of the channel, nicotine appears to induce a rapid desensitization of the nAChRs, closing the channel and resulting in a cessation of nicotine's effects. Research presented here will provide evidence of this secondary desensitization process in vivo by demonstrating nicotine's ability to induce acute tolerance in the discriminative stimulus (DS) paradigm. The ability of nicotine to elicit DS control of behavior was significantly reduced via challenge doses of (800, 1200, and 1600 ugjkg, s.c.) of nicotine administered 60-180 minutes prior to the training dose (400 ugjkg, s.c.). Eight out of twenty rats demonstrated this phenomena, with time and dose varying, suggesting that these effect may be contingent upon the individual rat studied. It appears that we have found a means of investigating cellular mechanisms in vivo using operant behavior.
5
Jones, Jeb. "Nicotine and responding maintained by conditioned reinforcers effects of two nicotinic antagonists /." [Gainesville, Fla.] : University of Florida, 2009. http://purl.fcla.edu/fcla/etd/UFE0041268.
Full text
6
Larsen, James D. "Nicotinic Acetylcholine Receptor Dependent Effects of Nicotine on HEK293T and HBO Cells." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5701.
Full textAbstract:
T2R receptors are the classical bitter taste receptors which detect and transduce bitter taste in a subset of taste receptor cells (TRCs). The TRPM5-dependent T2Rs are G-protein coupled receptors (GPCRs) and are linked to G protein, gustducin to initiate an intracellular signaling cascade for the transduction of bitter tastants. Nicotine is bitter. However, at present the transduction mechanisms for the detection of nicotine in are poorly understood. Previous studies from our laboratory using TRPM5 knockout (KO) mice demonstrated that the T2R pathway is insufficient in explaining the taste perception of nicotine. TRPM5 KO mice elicited chorda tympani (CT) taste nerve responses to nicotine, albeit significantly smaller than the wild type (WT) mice and still responded to nicotine as an aversive stimulus. Following addition of mecamylamine (Mec), a non-specific blocker of neuronal nicotinic acetylcholine receptors (nAChRs), CT responses to nicotine were partially inhibited in both WT and TRPM5 KO mice. Mec also decreases the aversive response to nicotine in both WT and TRPM5 KO mice. These studies led to the hypothesis that both a TRPM5-independent and TRPM5-dependent pathways are responsible for the detection and transduction of the bitter taste of nicotine in TRCs. The TRPM5-independent pathway most likely utilizes the nAChRs expressed in TRCs and function as bitter taste receptors for nicotine. We have subsequently demonstrated the expression of nAChRs in a subset of TRPM5-positive TRCs. However, this mechanism is not well understood in other cell types, particularly undifferentiated epithelial cells, such as HEK293T cells. The specific aims of this project were: (i) To identify which components of T2R-dependent taste reception as well as components of nAChRs are expressed in HEK293T cells; (ii) To determine if HEK293T cells co-express these components; (iii) To identify if exposure to nicotine modulates the expression of T2R and nAChR dependent components in HEK293T cells; (iv) To determine if TRCs express functional nAChR ion channels; and (v) To determine if nAChRs are involved in the release of neuropeptides, such as brain-derived neurotrophic factor (BDNF) in HEK293T cells. The data obtained in HEK293T cells was compared with parallel studies on adult cultured human fungiform taste cells (HBO) done independently by Dr. Jie Qian, a postdoctoral fellow in Dr. Vijay Lyall’s lab. The results of combined studies on HBO and HEK293T cells indicates that TRPM5-positive cells also co-express ionotropic nAChRs, comprising a and β subunits. The nAChRs are capable of forming ion pores and when stimulated by nicotine and create a parallel TRPM5-independent pathway for the detection of nicotine. Using molecular and immunocytochemical techniques, our results demonstrate that mRNAs and proteins for bitter taste receptors and downstream intracellular signaling components as well as subunits necessary for the formation of nAChRs are expressed in HBO and HEK293T cells. Results demonstrated that TRPM5-positive HEK293T cells co-expressed nAChR subunits throughout the entire population. Nicotine increased the influx of Ca2+ in a dose dependent manner, which was somewhat reduced by the addition of TRPM5 blocker, triphenylphosphine oxide (TPPO). Both mRNA and protein expression were altered in a biphasic pattern with a maximum increased observed at 0.5 µM nicotine with a decrease in expression at higher concentrations. The synthesis of neurotrophic factor BDNF, required for maturation of taste bud cells and their innervating nerves, increased in HEK293T cells exposed to nicotine, however, nicotine did not trigger the release of BDNF. These results were then compared and contrasted with HBO cells to better understand the comparative effects of nicotine on both undifferentiated and differentiated cells. The data on HBO cells is presented in the Appendix.
7
DiMaggio, Stassi. "Development of Novel Nicotinic Receptor Mediated Therapeutic Agents: Synthesis and Biological Evaluation of Novel Epibatidine Analogs and the First Total Synthesis of Anabasamine and Related Analogs." ScholarWorks@UNO, 2003. http://scholarworks.uno.edu/td/40.
Full textAbstract:
In an effort to search for a more selective, less toxic neuronal nicotinic acetylcholine receptor analgesic agent in comparison to epibatidine, a series of analogs with hybrid structures of epibatidine and ABT-594 were designed and synthesized. The 1-(pyridyloxymethyl)-7-azabicyclo[2.2.1]heptane ring systems were furnished via an intramolecular cyclization from a trans 1, 4 disubstitituted amino-cyclohexane derivative. The functionalized cyclohexane ring was formed via a [4+2] Diels-Alder cyclization reaction between the acetamidoacrylate and Danishefsky's diene. These 1- (pyridyloxymethyl)-7-azabicyclo[2.2.1]heptane ring systems were then tested in vitro as potential á4â2 nicotinic acetylcholine receptor ligands with high potency and selectivity. In addition, a series of rigid acetylcholine analogs were synthesized from cocaine to study the conformation of acetylcholine, the endogenous neurotransmitter at the nicotinic acetylcholine receptor. A stereoselective reduction of 2-tropinone led to the enantioselective synthesis of the desired acetoxytropane systems. These compounds were also tested in in vivo models for binding affinity and efficacy responses. Anabasamine, an alkaloid isolated from the Central Asian shrub, Anabasis aphylla, was synthesized for the first time. It was targeted due to interesting preliminary biological activity such as exhibiting anticholinesterase activity, anti-inflammatory activity, and facilitated an increase in hepatic alcohol dehydrogenase levels. Only preliminary studies were performed as anabasamine is limited in quantity due to its difficult isolation. A versatile synthetic methodology was developed for the synthesis of anabasamine and related nicotine analogs. This new methodology employed a pyridyl anion addition to valerolactone, for anabasamine, or butyrolactone for the nicotine analog, to afford 5-hydroxy-1-(6-methoxy-pyridin-3-yl)-pentan-1-one or 4-hydroxy-1-(6- methoxy-pyridin-3-yl)-butan-1-one, respectively. A reductive amination provided the piperidine ring moiety and a Suzuki coupling reaction introduced the bipyridyl moiety to anabasamine in five steps and 23% overall yield. In addition, this methodology was applied successfully to the synthesis of nicotine and other related analogs. In particular the synthesis of 6-methoxynicotine, a useful drug intermediate, was generated improving the yield from 16% over five steps to 54% over three steps.
8
Bowker, Katharine. "The effectiveness of nicotine replacement therapy during pregnancy : investigating the role of nicotine substitution, nicotine metabolism and pregnant smokers' experiences." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/32138/.
Full textAbstract:
Nicotine replacement therapy (NRT) is effective in non-pregnant populations at assisting smoking cessation, but there is no evidence that NRT can help pregnant smokers to stop. Nicotine metabolism increases during pregnancy, and so the nicotine dose delivered by NRT could be insufficient for ameliorating withdrawal symptoms. However, little is known about the level of nicotine substitution provided by NRT or the pattern of nicotine metabolism during pregnancy. Also low adherence to NRT may explain why NRT does not appear to be effective. The overall aim of this thesis was to increase understanding as to why NRT does not appear to be effective during pregnancy. The thesis consists of three studies. The first study involved analysing data on 33 pregnant participants from the NRT arm of a randomised control trial who had stopped smoking and were still using 15mg/16hr nicotine patches 1 month after quitting. Salivary cotinine levels when smoking at baseline were compared with levels on NRT at 1 month. Cotinine levels were lower than those achieved from smoking (median 98.5ng/ml while smoking and 62.8ng/ml while using NRT and remaining abstinent, p = 0.045). The second study involved 101 pregnant smokers, who were asked to provide saliva samples to measure NMR at 8-14 weeks, 18-22 weeks , 32-36 weeks gestation, 4 weeks postpartum and 12 weeks postpartum . Compared with NMR at 12 weeks postpartum, NMR was significantly higher at 18-22 weeks (26% higher, 95% CI 12% to 38%) and 32-36 weeks (23% higher, 95% CI 9% to 35%). There was no difference between the 8-14 weeks gestation or 4 weeks postpartum NMR and 12 weeks postpartum. The third study was a qualitative study that involved semi-structured telephone interviews with 14 pregnant smokers who had recently been prescribed NRT, but self-reported low NRT adherence or discontinuing treatment prematurely. Thematic analysis was used to analyse data. Most smoked regularly while using NRT and many used NRT to cut down their cigarette intake rather than to quit abruptly. Some were concerned that using NRT instead of smoking could actually increase their nicotine dependency or cause greater harm to the fetus, and consequently often underutilised NRT. This thesis supports the hypothesis that NRT at standard doses may be ineffective in pregnancy due to increased metabolism. The effectiveness of NRT may be hindered by the way in which NRT is used in pregnancy.
9
Vallaster, Markus Parzival. "Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/913.
Full textAbstract:
Environmental conditions imposed onto organisms during certain phases of their life cycles such as embryogenesis or puberty can not only impact the organisms’ own health, but also affect subsequent generations. The underlying mechanisms causing intergenerational phenotypes are not encoded in the genome, but the result of reversible epigenetic modifications. This work investigates in a mouse model the impact of paternal nicotine exposure on the next generation regarding addictive behavior modulation, metabolic changes, and molecular mechanisms. It provides evidence that male offspring from nicotine-exposed fathers (NIC offspring) is more resistant to lethal doses of nicotine. This phenotype is gender-specific and depends on short-term environmental challenges with low doses of nicotine prior to the LD50 application. The observed survival phenotype is not restricted to nicotine as drug of abuse, but also presents itself, when NIC offspring is challenged with a cocaine LD50 after acclimatization to low doses of either nicotine or cocaine. Functionally, NIC offspring metabolizes nicotine faster than control. Mechanistically, NIC offspring livers show global up-regulation of xenobiotic processing genes (XPG), an effect that is even more pronounced in primary hepatocyte cultures. Being known targets of Constitutive Androstane Receptor (CAR) and Pregnane X Receptor (PXR), these XPGs show higher baseline expression in naïve NIC offspring livers. Nicotine’s action on the brain’s reward circuitry does not appear to be of biological significance in our model system. Taken together, paternal nicotine exposure leads to a non-specific and conditional phenotype in male NIC offspring that may provide a general survival advantage against xenobiotic challenges.
10
Vallaster, Markus Parzival. "Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure." eScholarship@UMMS, 2008. http://escholarship.umassmed.edu/gsbs_diss/913.
Full textAbstract:
Environmental conditions imposed onto organisms during certain phases of their life cycles such as embryogenesis or puberty can not only impact the organisms’ own health, but also affect subsequent generations. The underlying mechanisms causing intergenerational phenotypes are not encoded in the genome, but the result of reversible epigenetic modifications. This work investigates in a mouse model the impact of paternal nicotine exposure on the next generation regarding addictive behavior modulation, metabolic changes, and molecular mechanisms. It provides evidence that male offspring from nicotine-exposed fathers (NIC offspring) is more resistant to lethal doses of nicotine. This phenotype is gender-specific and depends on short-term environmental challenges with low doses of nicotine prior to the LD50 application. The observed survival phenotype is not restricted to nicotine as drug of abuse, but also presents itself, when NIC offspring is challenged with a cocaine LD50 after acclimatization to low doses of either nicotine or cocaine. Functionally, NIC offspring metabolizes nicotine faster than control. Mechanistically, NIC offspring livers show global up-regulation of xenobiotic processing genes (XPG), an effect that is even more pronounced in primary hepatocyte cultures. Being known targets of Constitutive Androstane Receptor (CAR) and Pregnane X Receptor (PXR), these XPGs show higher baseline expression in naïve NIC offspring livers. Nicotine’s action on the brain’s reward circuitry does not appear to be of biological significance in our model system. Taken together, paternal nicotine exposure leads to a non-specific and conditional phenotype in male NIC offspring that may provide a general survival advantage against xenobiotic challenges.
11
McCarthy, Michael J. "Regulation of the endogenous opioid system by acute nicotine and nicotine withdrawal." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1076018422.
Full textAbstract:
Thesis (Ph. D.)--Ohio State University, 2004.<br>Title from first page of PDF file. Document formatted into pages; contains xiii, 172 p.; also includes graphics (some col.). Includes bibliographical references (p. 131-172 ). Available online via OhioLINK's ETD Center
12
Nelson, Christopher B., and Hans-Ulrich Wittchen. "Smoking and Nicotine Dependence." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-99925.
Full textAbstract:
This paper describes the distribution of dependence criteria and diagnoses in a sample of 14- to 24-year-olds from Munich, Germany (n = 3,021; 71% response rate), evaluates differences between nondependent and dependent smokers and examines associations of smoking with other substances, affective and anxiety disorders. Assessment was made using the M-CIDI. The lifetime prevalence of DSM-IV nicotine dependence in the total sample is 19%, rising to 52% among regular smokers. No gender differences were seen in the progression from regular smoking to nicotine dependence, although men were more likely than women to initiate regular use. Analysis of daily cigarette use identified a significant dose-response relationship with the number of endorsed DSM-IV dependence criteria with unsuccessful cut-backs being the most prevalent criterion. As compared to nondependent smokers, dependent smokers were more likely to associate negative health effects with smoking and to have a desire to change and attempt a change in their pattern of use. Regular use of nicotine was found to be significantly associated with other substance and nonsubstance disorders, although dependent regular use was more strongly associated with these disorders than nondependent regular use. These results indicate that daily smoking is a behavior which is resistant to change despite an expressed desire and repeated cut-back attempts. Although initiation of regular smoking among nonsmokers does not occur frequently after the early twenties, the risk for dependent smoking among regular users persists into adulthood and is associated with a range of mental disorders.
13
Alasmari, Fawaz Fayez. "Chronic Exposure to Electronic Cigarette Vapor-Containing Nicotine and Co-Exposure to Alcohol and Nicotine: Effects on Glial Glutamate Transporters, Nicotinic Receptors and Neurotransmitters." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1525349376479605.
Full text
14
Hildreth, Sherry Boston. "Investigation of Protein-Protein Interactions among Nicotine Biosynthetic Enzymes and Characterization of a Nicotine Transporter." Diss., Virginia Tech, 2003. http://hdl.handle.net/10919/29698.
Full textAbstract:
Alkaloids are a class of plant secondary metabolites produced in about 20% of plant families. Domesticated tobacco, Nicotiana tabacum produces nicotine as the predominant alkaloid. The biosynthesis of nicotine occurs exclusively in the roots of tobacco, yet accumulates in the leaves of tobacco where it is acts as a defense compound to deter insect herbivory. The research detailed in this dissertation addresses two aspects of nicotine physiology in tobacco: 1) an investigation of hypothesized protein-protein interactions among nicotine biosynthetic enzymes and 2) the characterization of a novel nicotine transporter.
A hypothesized metabolic channel including the two nicotine biosynthetic enzymes putrescine N-methyltransferase (PMT), N-methylputrescine Oxidase (MPO) and the S-adenosylmethionine (SAM) recycling enzyme S-adenosylhomocysteine hydrolase (SAHH) has been proposed. To further explore this hypothesis, protein-protein interactions among nicotine biosynthetic enzymes PMT, MPO and SAHH were investigated using yeast two-hybrid assays and co-immunoprecipitation experiments. The yeast two-hybrid was conducted as both a directed screen to detect interactions between the hypothesized metabolic channel members and as a library screen to detect interactions between hypothesized metabolic channel members and proteins from a tobacco root cDNA library.
Co-immunoprecipitation experiments were conducted using proteins produced in an in vitro transcription/ translation system and using native proteins from a tobacco root extract. The outcome of these experiments provided no further evidence of a nicotine metabolic channel and a discussion of the methods and outcomes of the experiments conducted is presented.
The nicotine uptake permease, NUP1, was identified in tobacco roots and was shown to preferentially transport nicotine when expressed in Schizosaccharomyces pombe. This report presents the characterization of tobacco plants and hairy roots with diminished NUP1 transcripts created by using RNAi. The NUP1-RNAi hairy roots and plants showed a decreased level of nicotine and the hairy root cultures displayed an altered distribution of nicotine from the root to the culture medium. Additionally NUP1-GFP was used to determine that NUP1 localized to the plasma membrane of tobacco BY-2 protoplasts. Potential models for the role of NUP1 in nicotine physiology will be discussed.<br>Ph. D.
15
Hildreth, Sherry B. "Investigation of Protein-Protein Interactions among Nicotine Biosynthetic Enzymes and Characterization of a Nicotine Transporter." Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/29698.
Full textAbstract:
Alkaloids are a class of plant secondary metabolites produced in about 20% of plant families. Domesticated tobacco, Nicotiana tabacum produces nicotine as the predominant alkaloid. The biosynthesis of nicotine occurs exclusively in the roots of tobacco, yet accumulates in the leaves of tobacco where it is acts as a defense compound to deter insect herbivory. The research detailed in this dissertation addresses two aspects of nicotine physiology in tobacco: 1) an investigation of hypothesized protein-protein interactions among nicotine biosynthetic enzymes and 2) the characterization of a novel nicotine transporter.
A hypothesized metabolic channel including the two nicotine biosynthetic enzymes putrescine N-methyltransferase (PMT), N-methylputrescine Oxidase (MPO) and the S-adenosylmethionine (SAM) recycling enzyme S-adenosylhomocysteine hydrolase (SAHH) has been proposed. To further explore this hypothesis, protein-protein interactions among nicotine biosynthetic enzymes PMT, MPO and SAHH were investigated using yeast two-hybrid assays and co-immunoprecipitation experiments. The yeast two-hybrid was conducted as both a directed screen to detect interactions between the hypothesized metabolic channel members and as a library screen to detect interactions between hypothesized metabolic channel members and proteins from a tobacco root cDNA library.
Co-immunoprecipitation experiments were conducted using proteins produced in an in vitro transcription/ translation system and using native proteins from a tobacco root extract. The outcome of these experiments provided no further evidence of a nicotine metabolic channel and a discussion of the methods and outcomes of the experiments conducted is presented.
The nicotine uptake permease, NUP1, was identified in tobacco roots and was shown to preferentially transport nicotine when expressed in Schizosaccharomyces pombe. This report presents the characterization of tobacco plants and hairy roots with diminished NUP1 transcripts created by using RNAi. The NUP1-RNAi hairy roots and plants showed a decreased level of nicotine and the hairy root cultures displayed an altered distribution of nicotine from the root to the culture medium. Additionally NUP1-GFP was used to determine that NUP1 localized to the plasma membrane of tobacco BY-2 protoplasts. Potential models for the role of NUP1 in nicotine physiology will be discussed.<br>Ph. D.
16
Jackson, Asti. "Investigating the Modulation and Mechanisms of α7 Nicotinic Acetylcholine Receptors in Nicotine Dependence". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4851.
Full textAbstract:
Tobacco dependence dramatically increases health burdens and financial costs. Limitations of current smoking cessation therapies indicate the need for improved molecular targets. Nicotine, the main addictive component of tobacco, exerts its dependency effects via nicotinic acetylcholine receptors (nAChRs). The homomeric α7 nAChR is one of the most abundant receptors found in the brain and has unique features in comparison to other nAChR subtypes such as high calcium permeability, low probability of channel opening, and a rapid desensitization rate. α7 nAChR agonists reduce nicotine's rewarding properties in the conditioned place preference (CPP) test and i.v. self-administration. Recently, the peroxisome proliferator-activated receptor type-α (PPARα) has been implicated as a downstream signaling target of the α7 nAChR in ventral tegmental area dopamine cells. It is unknown whether the intrinsic characteristics of the α7 nAChR and PPARα are involved in its attenuation of nicotine reward. Therefore, this dissertation sought to investigate the role of α7 nAChRs in a mouse model of nicotine CPP and nicotine withdrawal by 1) investigating the impact of pharmacological modulation of α7 nAChR function in nicotine dependence and 2) evaluating a possible role for PPARα as a downstream mediator of α7 nAChRs in nicotine dependence. Positive allosteric modulators (PAMs) and a silent agonist were used to investigate the role of α7 nAChR conformations. The utilization of the α7 nAChR Type I PAM NS1738, Type II PAM PNU120596, and silent agonist NS6740 provided insight about the probability of channel opening (NS1738, PNU120596), desensitization (PNU120596, NS6740), and modulation of the endogenous acetylcholine/ choline tone (NS1738, PNU120596) as it relates to the α7 nAChR in nicotine CPP and withdrawal. In addition, this dissertation sought to elucidate the role of the α7 nAChR and PPARα in nicotine dependence using pharmacological interventions. The results suggest that the role of the α7 nAChR in nicotine dependence is conformation-dependent and PPARα-mediated. This dissertation is the first to report PPARα-mediation of the effects of α7 nAChR in nicotine reward and attenuation of nicotine withdrawal signs by PPARα activation. This data supports the development of α7 nAChR agonists and PPARα activators as possible smoking cessation aids.
17
Carle, Carolyn M. "Nicotine Withdrawal Symptoms and Utilization of Nicotine Replacement Therapy in Critically Ill Smokers." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337876574.
Full text
18
Moraes, Ricardo Oliveira de [UNESP]. "Influência do laser em baixa intensidade no processo de reparo de de enxerto ósseo autógeno implantado em bloco na mandíbula de ratos modificados sistemicamente com nicotina: estudo histo- morfométrico." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/96151.
Full textAbstract:
Made available in DSpace on 2014-06-11T19:28:02Z (GMT). No. of bitstreams: 0
Previous issue date: 2010-08-18Bitstream added on 2014-06-13T20:57:34Z : No. of bitstreams: 1
moraes_ro_me_araca.pdf: 3762007 bytes, checksum: 9c2ec9715d0b3a85fbf41e3f7be91181 (MD5)<br>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)<br>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...<br>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)
19
Munhoz, Egberto. "Administração subcrônica de nicotina modifica as respostas neuroendócrina e neuroquímica induzidas pelo teste de natação forçada /." São Carlos, 2010. http://hdl.handle.net/11449/104039.
Full textAbstract:
Orientador: Cleopatra da Silva Planeta<br>Banca: Azair Liane Matos do Canto de Souza<br>Banca: Carlos César Crestani<br>Banca: Mirtes Costa<br>Banca: Marcelo Tadeu Marin<br>Resumo: O estresse, atualmente, é considerado um fator importante na fisiopatologia de muitos distúrbios psiquiátricos. Embora os efeitos do estresse agudo possam ser contrabalanceados por respostas adaptativas, o estresse intenso, repetido ou prolongado pode eliciar alterações neuronais duradouras que constituirão as bases de doenças psiquiátricas, como a depressão. Levantamentos epidemiológicos também mostram elevada prevalência de tabagistas entre pacientes com depressão maior. Estas altas taxas de comorbidade sugerem uma provável relação causal: pacientes com depressão proeminente procurariam a nicotina para alívio dos sintomas. Assim, este trabalho investigou as alterações neuroquímicas e neuroendócrinas mediadas pela nicotina na resposta de adaptação ao estresse, utilizando-se, para tanto, o teste modificado da natação forçada (TNF). Para tanto, ratos Wistar machos foram submetidos ao TNF (30 cm de água, 24 ± 1ºC) por 15 min e tratados (1, 19 e 23h) com nicotina (NIC: 0,5 mg/kg, sc), imipramina (IMI: 15 mg/kg, ip) ou salina (SAL). Uma hora após a última injeção, os animais foram reexpostos (5 min) à mesma cuba. Imediatamente após o teste, os animais foram sacrificados; o hipocampo dorsal (HD) e ventral (HV), hipotálamo (HT) e os núcleos dorsal (DR) e mediano (MR) da rafe foram coletados por punch para quantificação de 5-HT, 5-HIAA e NA por HPLC e o sangue, para quantificação da corticosterona plasmática por radioimunoensaio. O hipocampo total também foi utilizado para avaliar a expressão do receptor serotoninérgico 5-HT1A e do glicorreceptor (GR) por western blot. Ainda, avaliou-se o efeito da prazosina nas alterações neuroquímicas induzidas pelo TNF. O tratamento subcrônico com NIC e IMI reduziu em 39% e 50%, respectivamente, o parâmetro de imobilidade e aumentou em 52% e 66%, respectivamente, as contagens de escalada, em relação ao grupo... (Resumo completo, clicar acesso eletrônico abaixo)<br>Abstract: Stress is considered a key component in the pathophysiology of several psychiatric diseases. Although the effects of acute stress can be counterbalanced by adaptative responses, intense, repeated or prolonged stress can elicit long lasting neuronal alterations that are related to the occurrence of psychiatric disorders, such as depression. Epidemiological studies have also identified a high prevalence of smokers among depressive patients. These observations suggest a causal relationship: smoking is a self-medication effort to alleviate some symptoms of depression by nicotine. Then, this study investigated nicotine mediatedneurochemical and neuroendocrine alterations in the adaptation response to stress. The modified forced swmming test (FST), a protocol originally employed for screnning new antidepressant drugs, was employed. Male Wistar rats were placed individually into a container (30-cm of water, 24±1ºC, 15 min - pretest). Then animals received nicotine (0.5 mg/kg, s.c.), imipramine (15 mg/kg, i.p.) or saline injections at 1, 19 and 23h after the pretest. One hour after the injections, animals were placed in the same container for 5 min. Immediately after, the animals were sacrificed; dorsal (DH) and ventral (VH) hippocampus, hypothalamus (HT) and dorsal (DR) and median (MR) raphe nuclei were collected by punch for measurement of 5-HT, 5-HIAA and NA by HPLC (expressed in ng/mg tissue). Blood samples were collected for determination of plasma corticosterone levels by radioimmunoassay. The whole hippocampus was also used to evaluate the expression of the 5-HT1A serotoninergic receptor and glucocorticoid receptor by western blot. The effects of prazosin in TNF induced-neurochemical alterations was also evaluated. Nicotine and imipramine decreased in 39% and 50%, respectively, the immobility behavior and increased in 52% and 66%, respectively, the climbing scores, in relation to saline... (Complete abstract click electronic access below)<br>Doutor
20
Matheus, Henrique Rinaldi. "Avaliação da influência da quimioterapia com cisplatina ou 5-fluorouracil sobre o processo de reparo ósseo em implantes osseointegrados instalados em tíbias de ratos expostos ou não à nicotina /." Araçatuba, 2019. http://hdl.handle.net/11449/180853.
Full textAbstract:
Orientador: Juliano Milanezi de Almeida<br>Banca: Edilson Ervolino<br>Banca: Estevam Augusto Bonfante<br>Resumo: Objetivo: avaliar a influência da nicotina e dos agentes antineoplásicos Cisplatina (CIS) e 5-fluorouracil (5-FU) sobre os tecidos peri-implantares, bem como os efeitos desses agentes antineoplásicos sobre os tecidos peri-implantares em animais previamente expostos à nicotina. Material e métodos: 180 ratos machos (Wistar) foram randomizados para dois grandes grupos (n=90), NIC e SS, em seguida, para três subgrupos (n=30) de acordo com os agentes antineoplásicos. Receberam 0,5ml de solução de cloreto de sódio 0,9% (SS) ou 3 mg/kg de hemissulfato de nicotina (NIC), de acordo com cada grupo, 30 dias antes e 30 dias após a cirurgia. No dia 0, todos os animais receberam os implantes de titânio (DSP Biomedical®, 4 mm x 2,2 mm) nas tíbias direita e esquerda. Aos 30 dias após a cirurgia, as aplicações de SS e NIC foram interrompidas por 5 dias e, aos 35 e 37 dias, foram administrados os agentes antineoplásicos CIS, 5-FU ou 0,5 ml de SS, via intraperitoneal, respeitando intervalo de 48 h entre as aplicações. Para CIS, 5 mg/kg e 2,5 mg/kg, e para 5-FU, 60 mg/kg e 40 mg/kg, respetivamente. SS-SS: receberam SS via subcutânea e intraperitoneal. SS-CIS: receberam SS via subcutânea e CIS via intraperitoneal. SS-5FU: receberam SS via subcutânea e 5-FU via intraperitoneal. NIC-SS: receberam NIC via subcutânea e SS via intraperitoneal. NIC-CIS: receberam NIC via subcutânea e CIS via intraperitoneal. NIC-5FU: receberam NIC via subcutânea e 5-FU via intraperitoneal. Dez animais por grupo/período... (Resumo completo, clicar acesso eletrônico abaixo)<br>Abstract: Objective: to evaluate the influence of nicotine and the antineoplastic agents Cisplatin (CIS) and 5-fluorouracil (5-FU) over the peri-implant tissues, as well as the effects of these agents over peri-implant tissues in animals previously exposed to nicotine. Material and Methods: 180 male rats (Wistar) were initially randomized to two groups (n=90), NIC and SS. Then, to three subgroups (n=30) according to the protocol of antineoplastic agents. Received 0.5 ml of sodium chloride 0.9% (SS) or 3 mg/kg of nicotine hemissulfate (NIC) according to each group, subcutaneously, 30 days before and after surgical procedure for implants placement. At day 0, all animals received the titanium implants (DSP Biomedical®, 4 mm x 2.2 mm) in both right and left tibiae. At 30 days after surgery SS and NIC was interrupted, and at 35 and 37 days were intraperitoneally administered the antineoplastic agents CIS, 5FU or 0.5 ml SS, with 48 h interval between applications. For CIS, 5 mg/kg and 2,5 mg/kg, and 5-FU, 60 mg/kg and 40 mg/kg, respectively. SS-SS: received SS subcutaneously and intraperitoneally. SS-CIS: received SS subcutaneously and CIS intraperitoneally. SS-5FU: received SS subcutaneously and 5-FU intraperitoneally. NIC-SS: received NIC subcutaneously and SS intraperitoneally. NIC-CIS: received NIC subcutaneously and CIS intraperitoneally. NIC-5FU: received NIC subcutaneously and 5-FU intraperitoneally. Ten animals per group and period were euthanized at 50, 65 and 95 days after implants placement. The collected specimens were fixed in buffered formaldehyde solution 4% for 48h and assigned to ground section processing for analysis of bone/implant contact (BIC), or conventional histologic processing with demineralization and paraffin embedding for histometric analysis of percentage of newly-formed bone (PNFB) (Complete abstract electronic access below)<br>Mestre
21
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.
Full textAbstract:
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.
22
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.
Full textAbstract:
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.<br>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.
23
De, Villiers Sabina. "Active immunization against nicotine dependence." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-829-7/.
Full text
24
Thomas, Gareth Andrew Osbert. "Nicotine therapy for ulcerative colitis." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309526.
Full text
25
Mariner, Derek Christopher. "Nicotine - the mechanisms of uptake." Thesis, University of Surrey, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314871.
Full text
26
Tsai, Mui Chiung. "Metabolic studies of S-(-)-nicotine." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261707.
Full text
27
Young, Jared W. "Nicotine induced improvements in cognition : a possible role for the α7 nicotinic acetylcholine receptor". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/27731.
Full textAbstract:
Assessment of sustained attention in rodents can be performed using the 5-choice serial reaction-time (5-CSR) task; analogous to the continuous performance test used in man. A 5-CSR protocol was established which allowed the demonstration of nicotine-induced improvements in sustained attention in mice. In this task α7 nAChR knockout (KO) mice exhibited impaired acquisition and performance, providing additional evidence that this receptor may be a valid therapeutic target for cognitive enhancement. In order to investigate the role of nAChR manipulation on working memory, the odour span task, a test of olfactory working memory capacity, was established in mice. Nicotine administration did not improve performance of C57B1/6J mice probably as a consequence of ceiling effects. Transgenic mice over-expressing human caspase-3 (hc-3) displayed a robust impairment in the task that was attenuated by nicotine administration. Moreover α7 nAChR KO mice exhibited impaired acquisition and performance in the task but in a different pattern to that of the hc-3 mice. This pattern may reflect an impaired ability to attend to the task as opposed to a working memory deficit alone. These demonstrations provide further support for a role of the α7 nAChR in cognition. Tg2576 mice represent the best well characterised transgenic model of AD, however there remains a dearth of information on their attentional and olfactory capabilities. The mice exhibited a deficit in sustained attention in the 5-CSR task, as well as an age-related impairment in the odour span task. In conclusion the development of the 5-CSR task for mice was used to identify a nicotine-induced improvement in normal mice and impaired performance in α7 KO and Tg2576 mice. In summary these data provide some evidence for a role of the α7 nAChR in nicotine-induced improvement in cognition, and with the tasks developed provide new tools for the assessment of putative cognitive enhancing compounds.
28
Claude, J. P. "Nutrition minérale et régulation de la synthèse de la nicotine chez Nicotiana tabacum L." Doctoral thesis, Universite Libre de Bruxelles, 1985. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213637.
Full text
29
Barik, Jacques. "Nicotinic modulation of cellular and molecular processes : impact of chronic nicotine and its withdrawal." Thesis, University of Bath, 2006. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428384.
Full textAbstract:
There is a growing body of evidence that nicotinic acetylcholine receptors (nAChR) within the central nervous system (CNS) modulate a variety of cellular processes, including neurotransmitter release and signalling cascades. nAChR are ligand gated cation channels. The large diversity of nAChR subunits gives rise to functional homoand hetero-pentameric nAChR, and dictates their distinct intrinsic pharmacological properties. A further degree of complexity is reached by the non-uniform pattern of distribution of nAChR through the CNS. This research project has focused on several aspects of the modulatory actions of nAChR in different brain regions. The first part of the project examined the ability of nAChR to modulate [3H]dopamine and [3H]noradrenaline release in striatal and hippocampal rat brain slices respectively, which preserve some of the existing neuroanatomical connections enabling the investigation of neurotransmitter crosstalk. In both regions a7 nAChR were inferred to indirectly modulate catecholamine release via enhancement of glutamate release. In contrast, a7 nAChR appeared to modulate an additional GABAergic component solely within the hippocampus. We secondly investigated the impact of a continuous nicotine exposure and its withdrawal in vivo on these two neurotransmitter interplays assessed in vitro. In both the dopaminergic and the noradrenergic systems, we found a consistent, selective and transient functional enhancement of a7 nAChR-evoked [³H]catecholamine release at the 3 days withdrawal period following continuous nicotine exposure. This finding was further examined using a7 nAChR knock out mice. Prolonged exposure to abused drugs, including nicotine, has been proposed to cause long-lasting neuroadaptations. We next studied in vivo the effects of various modes (acute, and intermittent or continuous for 14 days) of nicotine administration on three key proteins (DARPP-32, Elk-1 and FosB) of the dopaminergic signalling. The route of nicotine delivery differentially altered the phosphorylation status and/or protein levels. In addition, sustained changes during nicotine withdrawal were only observed following continuous drug administration, but not repeated injections. Finally, we aimed at understanding in a simpler system the impact on nAChR function of chronic nicotine with respect to agonist binding and receptor activation. To reach this goal, we exposed the SH-SY5Y cell line to nicotine or the prototypical allosteric potentiating ligand, galantamine, and measured the functional outcome of such treatments. Data indicate dissociation between upregulation of nAChR numbers and alteration of nAChR function. These studies have extended our understanding of the modulatory properties of nAChR, with emphasis on the differential impacts of acute and prolonged nicotine administration on nAChR activation, and the downstream cellular processes they modulate.
30
Manzano, Beatriz Martins [UNESP]. "Variabilidade da frequência cardíaca como ferramenta de análise da função autonômica de tabagistas: revisão de literatura e estudo do plot de Poincaré." Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/87320.
Full textAbstract:
Made available in DSpace on 2014-06-11T19:22:49Z (GMT). No. of bitstreams: 0
Previous issue date: 2009-12-11Bitstream added on 2014-06-13T20:09:54Z : No. of bitstreams: 1
manzano_bm_me_prud.pdf: 326376 bytes, checksum: 0b7d0d1cb3bdf834e64a73541c8ddedd (MD5)<br>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)<br>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...<br>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)
31
Zirger, Jeffrey M. "Cloning, Expression and Functional Analysis of the Zebrafish Neuronal Nicotinic Acetylcholine Receptor." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1052847984.
Full text
32
Stafford, Alexandra M. "alpha6 beta2 subunit containing nicotinic acetylcholine receptor contributions to abuse-related effects of nicotine and alcohol." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4778.
Full textAbstract:
Pharmacotherapies for tobacco and alcohol cessation are only modestly successful, so it is important to better understand mechanisms underlying their use and abuse. The overarching goal of this research is to assess a6b2 subunit containing nicotinic acetylcholine receptor (a6b2*nAChR; *denotes possible assembly with other subunits) contributions to abuse-related effects of nicotine and alcohol. In the absence of a6b2*nAChR-selective agonists, a6b2*nAChR gain-of-function (a6L9’S) mice provide a tool for selective activation of a6b2*nAChRs. Using the a6L9’S mice together with nicotine doses sub-threshold for stimulation of native nAChRs, these studies tested the hypothesis that activation of a6b2*nAChRs is sufficient to promote neurochemical and behavioral effects relevant to nicotine addiction. Intracranial infusions of an a6b2*nAChR-selective antagonist further tested the neuroanatomical locus of a6b2*nAChR contributions to mesolimbic dopamine (DA) release and nicotine reward behavior. Our in vivo microdialysis and nicotine conditioned place preference (CPP) studies reveal that stimulation of a6b2*nAChRs on ventral tegmental area (VTA) DA neurons, as well as on DA terminals in the nucleus accumbens (NAc) shell support nicotine reward. VTA a6b2*nAChR stimulation is required for elevated basal NAc DA levels in a6L9’S mice, who also show elevated nicotine CPP. These studies also showed elevated anxiety-like behavior in a6L9’S mice, but no change in a6 subunit null mutant (a6KO) mice to suggest that elevated cholinergic tone at a6b2*nAChRs promotes anxiety-like behavior. To better define the molecular make-up of a6b2*nAChRs supporting nicotine reward and anxiety-like behavior, these studies crossed a6L9’S to a4 subunit knockout mice to differentiate (non-a4)a6b2* and a4a6b2*nAChR contributions. (non-a4)a6b2*nAChRs appear to promote nicotine reward behavior, while the a6b2*nAChR subtype that regulates anxiety-like behavior depends on the anxiety assay. Finally, these studies developed a mouse model of oral operant ethanol (EtOH) self-administration and assessed EtOH reinforcement in a6 heterozygous (a6HET) and a6KO mice to characterize the role of a6b2*nAChRs in EtOH reinforcement. EtOH self-administration was similar to wild type mice in a6KO mice, but not a6HET mice, suggesting that expression of a6b2*nAChRs modulates EtOH reinforcement. Together, these preclinical studies implicate a6b2*nAChRs in various abuse-related effects of nicotine and alcohol, identifying this receptor as a potential therapeutic target for treatment of dependence.
33
Jackson, Kia. "Identification of Pharmacological and Molecular Mechanisms involved in Nicotine Withdrawal." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1616.
Full textAbstract:
Tobacco dependence is the leading cause of preventable death in the United States. Despite currently available smoking cessation therapies, there is a high rate of relapse in smoking among those attempting to quit. While the somatic signs of nicotine withdrawal (insomnia, increased appetite, weight gain) contribute to the continuation of smoking behavior, it has been hypothesized that the affective signs (depression, anxiety, craving, irritability) are greater motivators of relapse and continued tobacco use. There are few studies that assess the molecular and receptor-mediated mechanisms of nicotine withdrawal; therefore, our studies focus on identifying the nicotinic acetylcholine receptor (nAChR) subtypes and post-receptor calcium-dependent mechanisms involved in nicotine withdrawal behaviors. Using precipitated, spontaneous, and conditioned place aversion (CPA) models, we measured physical and affective signs of nicotine withdrawal in mice. Our data show that major nAChR subtypes have differential roles in nicotine withdrawal. Additionally, our results suggest a behavioral relevance for L-type calcium channels in physical nicotine withdrawal signs, while calcium/calmodulin dependent protein kinase II (CaMKII) appears to be involved in both physical and affective withdrawal behaviors. Additionally, we conducted biochemical studies in the ventral tegmental area (VTA) and nucleus accumbens (NAc) to examine the relationship between altered withdrawal behavioral responses and calcium-dependent molecular mechanisms that contribute to nicotine withdrawal behaviors. Our results suggest an important role for β2-containing nAChRs in nicotine-withdrawal induced decreases in CaMKII and synapsin I function in the NAc. Overall, our studies implicate a critical role for the α4α6β2* nAChR subtype in the behavioral and molecular aspects of nicotine withdrawal, thus aiding in the elucidation of nAChR subunits and mechanisms that contribute to nicotine withdrawal behaviors. The current studies are imperative for generating more successful smoking cessation therapies.
34
Penton, Rachel E. "Changes in hippocampal excitability during withdrawal from chronic nicotine." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/penton.pdf.
Full text
35
Henzelin-Nkubana, Céline. "Elaboration d'un vaccin anti-nicotine : développement et synthèse de conjugués immunogéniques de dérivés de la nicotine /." [S.l.] : [s.n.], 2003. http://library.epfl.ch/theses/?nr=2682.
Full text
36
Middleton, Lisa Sue. "Nicotine receptor modulation of dopamine transporters." Lexington, Ky. : [University of Kentucky Libraries], 2005. http://lib.uky.edu/ETD/ukyphsc2006d00383/Middleton.pdf.
Full textAbstract:
Thesis (Ph. D.)--University of Kentucky, 2005.<br>Title from document title page (viewed on March 2, 2006). Document formatted into pages; contains vii, 264 p. : ill. Includes abstract and vita. Includes bibliographical references (p. 196-260).
37
Keyworth, Helen. "Nicotine addiction : behavioural and neurochemical mechanisms." Thesis, University of Surrey, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606818.
Full textAbstract:
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.
38
Millen, D. Leslie C. "The recovery of nicotine from tobacco." Thesis, Queen's University Belfast, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356893.
Full text
39
Hahn, Britta. "Mechanisms of nicotine-induced attentional enhancement." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400578.
Full text
40
Wood, Teresa Lynne. "Biobehavioral aspects of adolescent nicotine dependence /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486401895209856.
Full text
41
Asgaard, Gregory L. "Modulation of affective priming by nicotine /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456288431&sid=4&Fmt=2&clientId=1509&RQT=309&VName=PQD.
Full text
42
Pashmi, Ghazaleh. "Immunotherapy approach to combat nicotine addiction." Thesis, University of Bath, 2004. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419340.
Full textAbstract:
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.
43
Alkhlaif, Yasmin. "IMPACT OF CHEMOTHERAPY ON NICOTINE DEPENDENCE." VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5175.
Full textAbstract:
Although cigarette smoke has been implicated in a causal relationship with various types of cancers, around 62% of all cancer patients are current smokers, recent quitters, or former smokers. While most patients who are smokers are motivated to quit after cancer diagnosis, 25 -30% of these patients continue to smoke. Furthermore, most quitters relapse after 2-3 years of post-chemotherapy. This represents a major health concern since several clinical studies revealed that perpetuation of smoking in cancer populations attenuates patient's well-being and quality of life. Smoking may impair healing, attenuate the efficacy of chemotherapy, increase the disease complications and diminish survival rates. However, the factors that involved in nicotine dependence in cancer patients are poorly understood. xii According to human research, it was suggested that tumor site, impact of cancer therapy and disease prognosis could be responsible of continuation of tobacco smoking among cancer patients and survivors. Recently, chemotherapy was shown to cause emotional deficits in humans (anxiety, insomnia and depression) and animals. In this project, we focused on the chemotherapeutic agent, paclitaxel, because it is widely used to treat solid tumors such as lung, head, neck and breast cancer. We previously reported that paclitaxel induced general affective deficits in mice such as anhedonia, anxiety and depression-like behaviors. We therefore hypothesized that the chemotherapeutic agent, paclitaxel may alter the rewarding and withdrawal properties of nicotine. We investigated the impact of paclitaxel on spontaneous nicotine withdrawal and nicotine reward in C57BL/6J mice by using variety of behavioral tests. Our findings showed that paclitaxel worsened the somatic and affective signs of nicotine withdrawal in male mice as well as attenuated of nicotine reward in the CPP assay. These behavioral changes were not due to an impact of nicotine metabolism by paclitaxel. Overall, paclitaxel changed the behaviors during nicotine withdrawal and reward and that suggested changing in the smoking behavior after exposure to chemotherapy.
44
Buelow, Melissa T. "The Influence of Nicotine Craving and Personality Characteristics on Risky Decision Making in Nicotine Dependent College Students." Ohio University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1246932131.
Full text
45
Kleykamp, Betha A. "The Effects of Transdermal Nicotine on Tobacco/Nicotine Withdrawal and Concurrently Administered Cigarettes in Women and Men." VCU Scholars Compass, 2007. http://scholarscompass.vcu.edu/etd/1218.
Full textAbstract:
Transdermal nicotine (TN) is a smoking cessation pharmacotherapy thought to work by suppressing tobacco/nicotine withdrawal and reducing the effect of a concurrently smoked tobacco cigarette. Clinical trials suggest that TN may be less efficacious for women. This study explored the possibility of gender differences in response to transdermal nicotine in 54 women and 70 men. Participants completed four within-subject, double-blind, randomized sessions corresponding to 0, 7, 14, and 21 mg TN and 4-hrs after TN application smoked an own-brand cigarette. Prior to session onset participants completed ≥ 8 hours of verified tobacco cigarette abstinence (i.e., expired air carbon monoxide levels ≤ 10 ppm). Subjective and physiological measures were administered throughout each session, and cognitive performance and smoking behavior were assessed at time points related to the smoking opportunity.Results revealed that there were few significant effects involving the gender factor across withdrawal suppression and concurrent smoking outcomes (13 significant gender-related effects out of 338 possible; 3.9%). Women were more sensitive to some of the direct effects of nicotine in the 21 mg TN condition (e.g., increased ratings of "Nauseous"). However, for women and men TN suppressed some of the signs and symptoms of withdrawal and attenuated smoking-related increases in heart rate and subjective effects that might be indicative of the positive reinforcing properties of smoking (e.g., "Was the cigarette satisfying?"). In addition, for women and men, TN did not attenuate properties of smoking that might be negatively reinforcing (e.g., smoking- induced reductions in withdrawal symptoms). Thus, although this study does not shed light on clinical observations that TN is less effective for women, results suggest that NRT might be more efficacious if combined with other interventions that supplement the withdrawal suppressing effects of TN and reduce the negative reinforcing qualities of smoking.
46
Hiler, Marzena M. "Electronic Cigarette User Plasma Nicotine Concentration and Puff Topography: Influence of Liquid Nicotine Concentration and User Experience." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4613.
Full textAbstract:
Electronic cigarettes (ECIGs) aerosolize an often nicotine-containing solution for user inhalation. ECIG nicotine delivery may depend on liquid nicotine concentration and user puffing behavior (topography). This study examined the relationship among liquid nicotine concentration, puff topography, and plasma nicotine concentration. Thirty-three ECIG-experienced and 31 ECIG-naïve individuals completed four laboratory sessions that differed by ECIG liquid nicotine concentration (0, 8, 18, or 36 mg/ml). A 3.3 volt “eGo” ECIG battery attached to a 1.5 Ohm dual coil “cartomizer” filled with 1 ml of 70% propylene glycol/30% vegetable glycerin nicotine liquid was used in two ECIG-bouts (10 puffs; 30 s IPI). Plasma nicotine concentration, puff topography, and HR were evaluated. Some ECIG/liquid combinations can deliver physiologically active doses of nicotine to users, and nicotine delivery depends on liquid nicotine concentration and user puffing behavior. Liquid contents, device characteristics, and user behavior should be considered when regulating ECIGs.
47
Maier, Sheila Irene Bridget. "Melatonin receptor knockout mice have an increased physiological reaction to nicotine and increased voluntary oral nicotine consumption." Connect to online resource, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1453515.
Full text
48
Windvogel, Shantal Lynn. "An investigation into the effect of maternal exposure to nicotine and copper on neonatal lung development." Thesis, University of the Western Cape, 2006. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_3411_1194336120.
Full textAbstract:
<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>
49
Freitas, André Luiz Nunes. "A susceptibilidade à nicotina e etanol é afetada pela exposição à nicotina, fumaça de cigarro e etanol durante o período gestacional: alterações comportamentais e eletrofisiológicas no período pós-natal de camundongos." Universidade do Estado do Rio de Janeiro, 2014. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=8575.
Full textAbstract:
Conselho Nacional de Desenvolvimento Científico e Tecnológico<br>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.<br>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.
50
Manzano, Beatriz Martins. "Variabilidade da frequência cardíaca como ferramenta de análise da função autonômica de tabagistas : revisão de literatura e estudo do plot de Poincaré /." Presidente Prudente : [s.n.], 2009. http://hdl.handle.net/11449/87320.
Full textAbstract:
Orientador: Dionei Ramos<br>Banca: Moacir Fernandes de Godoy<br>Banca: Ercy Mara Cipulo Ramos<br>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)<br>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)<br>Mestre