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Vitay, Julien. "On the role of dopamine in motivated behavior". Doctoral thesis, Universitätsbibliothek Chemnitz, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:ch1-qucosa-213695.
Pełny tekst źródłaNeuronale Modelle nach dem Vorbild des Gehirns bieten die Möglichkeit intelligente, kognitive Prozesse nicht nur besser zu verstehen, sondern sie stellen auch eine vielversprechende Lösung dar, um eine Gehirn-ähnliche künstliche Intelligenz für Wahrnehmung und Verhaltensweisen zu erreichen, die mit natürlicher Intelligenz konkurrieren kann. Eine entscheidende Eigenschaft von intelligentem Verhalten ist Motivation, definiert als der Anreiz mit der Welt zu interagieren, um bestimmte Ziele zu erreichen, sei es extrinsisch (Belohnungen wie Nahrung oder Geld zu erhalten oder die Vermeidung von Schmerzen) oder intrinsisch (die Neugier zu befriedigen, Spaß zu haben). Im menschlichen Gehirn basiert motiviertes oder zielgerichtetes Verhalten auf einem Netzwerk von verschiedenen Strukturen, einschließlich des präfrontalen Cortex, der Basalganglien und des limbischen Systems. Dopamin, ein Neurotransmitter, welcher der Belohnungsverarbeitung zugeordnet wird, spielt eine zentrale Rolle bei der Koordination der Aktivität in diesem Netzwerk. Es strukturiert die Verarbeitung in High-Level-kognitiven Bereichen entlang eines limbischen-assoziativ-motor Gradienten und beinflusst die Lernfähigkeit des gesamten Systems. In dieser Habilitation, präsentiere ich biologisch motivierte neuronale Modelle, die die Rolle von Dopamin in der visuellen Objektkategorisierung und Gedächtnisabruf (Vitay and Hamker, 2008), Reinforcement Lernen und Aktionsauswahl (Vitay and Hamker, 2010), Aktualisierung, Lernen und Aufrechterhaltung von Arbeitsgedächtnis (Schroll et al., 2012) und Timing Prozessen (Vitay and Hamker, 2014) untersuchen. Diese Modelle beschreiben Mechanismen, durch die das dopaminerge System kognitives und emotionales Verhalten reguliert: bistabile Verarbeitungsmodi in der Hirnrinde, Plastizität und Modulation der synaptischen Übertragung, Zuweisung von kognitiven Ressourcen und Signalisierung von relevanten Ereignissen. Schließlich beschreibe ich einen neuronalen Simulator, der in in der Lage ist, eine Vielzahl von neuronalen Modellen effizient auf parallelen Architekturen zu simulieren (Vitay et al., 2015)
Burke, Mark 1975. "Factors that influence the dopamine neuron as revealed by dopamine transporter expression". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85892.
Pełny tekst źródłaAlterations in the activity of monoamine oxidase (MAO), a degradative enzyme that plays an important role in regulating levels of monoamine transmitters, may have a profound effect on brain development. The present study investigates relative DA and serotonin innervation of cortical and subcortical areas, measured by DAT and SERT densities, following MAO inhibition (A or B or A+B) in mice throughout gestation and early post-natal development. DAT binding was unaltered within the nigrostriatal pathway. The most significant finding reported here is that the combined MAO-A+B inhibition significantly reduced SERT binding by 25% in both the cortex and raphe nucleus. Lower levels of SERT binding were apparent during the early post-natal period (PND 14), a period during which pups were still exposed to MAO inhibitors in the dam's milk, but also persisted into later life (PND's 35 and 90) after inhibitors were no longer being administered. Persistent effects were restricted to cortex and raphe, suggesting a relative vulnerability of these regions to alterations in monoamine transmitter levels during development.
The second study presents data demonstrating that Hx delivered intracerebroventricularly significantly reduces the number of tyrosine hydroxylase immunoreactive cells (TH-ir) in the substantia nigra by 22% and 30%, at 7 and 21 days, respectively. After 3 days of Hx administration, striatal DA and serotonin were elevated over control levels by 22% and 25%, respectively, but returned to control levels by 7 days. The serotonin metabolite 5-HIAA was elevated after 3 days of Hx, but levels of DA metabolites were not different from control. Locomotion, a behavior thought to be related to DA transmission, was elevated following Hx treatment, as were presynaptic markers of the DA system such as DAT and TH protein levels. The persistent reduction in TH positive cell numbers suggests that Hx damages or kills DA neurons. The increase in intracellular DA at early time points suggests that Hx might interfere with DA release, possibly by temporarily inactivating DA neurons. These findings are consistent with the hypothesis that Hx, a purine significantly elevated in blood and CSF of Lesch-Nyhan patients, maybe involved in DA dysfunction.
Studies on alcohol abuse have focused on the mesolimbic DA pathway and the serotonergic influence within this pathway. Here we report that abstinent binge-drinking monkeys have significant reductions of SERT binding, and to a lesser extent, DAT binding in the midbrain region, while abstinent heavy-drinking subjects have elevated levels of DAT binding, as compared to controls. Both mesolimbic and nigrostriatal pathways are affected. CSF levels of both HVA and 5-HIAA substantiate the neuroanatomical differences between binge- and heavy-drinking vervets. Taken together, these findings provide a neurochemical profile with which to further distinguish subtypes of alcohol-preferring vervet monkeys.
Bergman, Olle. "On the influence of dopamine-related genetic variation on dopamine-related disorders /". Göteborg : Department of Pharmacology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, 2009. http://hdl.handle.net/2077/21077.
Pełny tekst źródłaKim, Douglas S. "Dopamine and adenosine receptor function in adult and developing dopamine-deficient mice /". Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/5063.
Pełny tekst źródłaHall, A. "Irreversibly binding dopamine analogues". Thesis, University of East Anglia, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355531.
Pełny tekst źródłaCaravona, Natalia Filomena. "Behaviour disorders dopamine-related". Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1042.
Pełny tekst źródłaMartin-Iverson, Mathew Thomas. "The effect of a dopamine antagonist and an agonist on rats’ perception of reward quantity : an examination of the anhedonia hypothesis". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25938.
Pełny tekst źródłaMedicine, Faculty of
Graduate
Erickson, Crystal. "Dopamine's role in risk taking: a specific look at dopamine deficiency and gambling". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110501.
Pełny tekst źródłaIntroductionLe système dopaminergique mésolimbique est connu pour son importance dans la prise de décision, lié au mécanisme de la récompense. Un disfonctionnement de ce système influe sur l'impulsivité, qui peut être considéré comme une forme anormale de la prise de décisions. De nombreux désordres neuropsychiatriques, tel que l'addiction aux drogues, l'obésité et le jeu compulsif, sont caractérisés par une sur-sensibilité à la récompense et une insensibilité aux conséquences négatives.Le traitement des patients atteint de la maladie Parkinson, par des substituts en Dopamine peut entrainer, de manière inhabituelle, des comportements à risques, tel que des pathologies liées aux jeux d'argent ou des impulsions sexuelles. Nous posons deux questions : 1) Existent-ils des anormalités sous-jacentes dans un procédé neuronal de prise de décisions chez les patients atteints de Parkinson qui développent des désordres impulsifs ? 2) Quel rôle joue la Dopamine dans la prise de décisions à risque chez des jeunes sujets sains.MéthodesL'Expérience 1 : Nous avons utilisé l'Imagerie par Résonance Magnétique Fonctionnelle chez des patients atteints de Parkinson, avec désordre impulsif (n=11), comparé a deux groupes témoins : Groupe de patients parkinsoniens sans troubles compulsif, (n=12) et sujets-control non-atteint du même âge (n=11).Expérience 2 : Nous avons utilisé la méthode "Acute phenylalanine/tyrosine depletion (APTD)" [pour réduire le niveau Dopamine], l'Imagerie par Résonance Magnétique Fonctionnelle et la Tomographie par Emission de Positons chez des sujets sains âgés de 18 a 30 ans (n=17) ainsi que des tests d'impulsivité et d'apprentissage.RésultatsExpérience 1 : (1) La prédisposition aux désordres impulsifs est relié a des différences de personnalité, et dans l'évaluation du risque financier. (2) Le groupe PD-avec troubles compulsifs révèle un disfonctionnement dans la pondération des pertes relative aux gains, de manière comportementale et neuronale. (3) L'erreur dans la prédiction de la récompense n'est pas nécessaire dans le développement ou maintien des addictions comportementales. Les irrégularités dans l'évaluation du risque et de la récompense par le cortex insulaire seraient à l'origine du développement d'un désordre impulsif dans la maladie de Parkinson.Expérience 2 : (1) La diminution de la Dopamine dans le cerveau a augmenté l'aversion à la perte, ainsi que l'aptitude à apprendre les conséquences négatives; plus la diminution de la Dopamine (déplétion) est importante, telle que mesurée par la TEP, plus cela améliore l'évaluation de la punition (2). Les scores élevés d'impulsivité corrèlent avec le niveau de récepteurs D2, qui pourraient indiquer une faible réponse tonique des neurones dopaminergiques et une tendance vers une haute réponse phasique de ces neurones. (3) Le signal BOLD corrèle avec la valeur attendue et l'erreur de prédiction de la récompense, de façon bilatérale dans le striatum ventral. Cette corrélation augmente de manière significative après la réduction de la Dopamine, suggérant que le signal BOLD dans cette même région ne résulte pas directement de la libération de Dopamine.Conclusion: Il y a quatre conclusions principales: (1) le signal BOLD dans le striatum ventral peut être due à d'autres neurotransmetteurs que la dopamine, (2) le risque et l'aversion à la perte dependent du niveau de Dopamine, (3) l'impulsivité est causée par une haute réponse phasique de Dopamine, enfin (4) apprendre à éviter des choix mal-adaptés depend des niveaux de Dopamine et des récepteurs D2. Ce projet fournit les bases d'une meilleure compréhension de la récompense et de l'aversion à la perte qui contrôle la prise de risque, l'apprentissage de la récompense et l'impulsivité.
Sugamori, Kim S. "The dopamine D1C receptor, expansion and origin of the dopamine D1 receptor family". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0001/NQ41320.pdf.
Pełny tekst źródłaStevenson, Carl W. "Basolateral amygdala dopamine modulation of medial prefrontal cortical and nucleus accumbens dopamine function". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84846.
Pełny tekst źródłaClements, Michael. "Control of striatal dopamine transmission by cocaine and nicotine : acetylcholine and dopamine interactions". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496839.
Pełny tekst źródłaPhillips, Gavin. "Dopamine and reward : effects of dopamine antagonist drugs on operant and consummatory behaviours". Thesis, London Metropolitan University, 1990. http://repository.londonmet.ac.uk/3064/.
Pełny tekst źródłaObray, J. Daniel. "Peripheral Dopamine 2 Receptors Both Modulate Central Dopamine Release and Adopt in a Similar Manner to that of Central Dopamine 2 Receptors". BYU ScholarsArchive, 2020. https://scholarsarchive.byu.edu/etd/8983.
Pełny tekst źródłaWallace, Raye Ann. "The interaction of structural analogs of dopamine, chlorpromazine and sulpiride with striatal dopamine receptors /". The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487586889186522.
Pełny tekst źródłaLi, Libin Reith Maarten E. A. "Regulation of the human dopamine transporter". Normal, Ill. Illinois State University, 2002. http://wwwlib.umi.com/cr/ilstu/fullcit?p3064534.
Pełny tekst źródłaTitle from title page screen, viewed February 3, 2006. Dissertation Committee: Maarten E.A. Reith (chair), Hou Tak Cheung, Paul A. Garris, Stephen M. Lasley, Brian J. Wilkinson. Includes bibliographical references and abstract. Also available in print.
Xu, Cen Reith Maarten E. A. "Cocaine and the dopamine transporter". Normal, Ill. Illinois State University, 1996. http://wwwlib.umi.com/cr/ilstu/fullcit?p9721400.
Pełny tekst źródłaTitle from title page screen, viewed May 30, 2006. Dissertation Committee: Maarten E. A. Reith (chair), Hou Tak Cheung, John W. Dailey, Robert L. Preston, Brian J. Wilkinson. Includes bibliographical references and abstract. Also available in print.
Fedorow, Heidi School of Medical Science UNSW. "Neuromelanin in human dopamine neurons". Awarded by:University of New South Wales. School of Medical Science, 2005. http://handle.unsw.edu.au/1959.4/32717.
Pełny tekst źródłaMcManus, Karen. "Dopamine and antidepressant drug action". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq29076.pdf.
Pełny tekst źródłaSchilaty, Nathan Dan. "Alcohol Modulation of Dopamine Release". BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/5826.
Pełny tekst źródłaNoronha, Emmanuelle Coelho. "AÃÃo de drogas agonistas e antagonistas dos sistemas colinÃrgico e dopaminÃgico: estudo comportamental e neuroquÃmico em corpo estriado de rato". Universidade Federal do CearÃ, 2005. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=277.
Pełny tekst źródłaNo presente trabalho, foi avaliado a interaÃÃo entre os sistemas dopaminÃrgico e colinÃrgico atravÃs do estudo dos efeitos comportamentais (campo aberto e catalepsia) e neuroquÃmicos (densidade de receptores dopaminÃrgicos (D1 e D2-sÃmile) e muscarÃnicos (M1+M2-sÃmile) em corpo estriado de rato. As seguintes drogas foram utilizadas: mazindol (agonista dopaminÃrgico indireto), apomorfina (agonista dopaminÃrgico D1-sÃmile e D2-sÃmile), pimozida (antagonista dopaminÃrgico D2-sÃmile), SCH 23390 (antagonista dopaminÃrgico D1-sÃmile), pilocarpina (agonista muscarÃnico M1-sÃmile), carbacol (agonista muscarÃnico M2-sÃmile), pirenzepina (antagonista muscarÃnico M1-sÃmile), atropina (antagonista muscarÃnico M1 e M2 nÃo seletivo), clozapina (neurolÃptico atÃpico). Os resultados mostraram que a pimozida e o carbacol, sozinhos ou associados, causaram um aumento da resposta catalÃptica e uma diminuiÃÃo da atividade locomotora. O mazindol tambÃm aumentou a atividade locomotora. Carbacol, nas menores doses, e o mazindol aumentaram a densidade de receptores D1-sÃmile. A pimozida e a atropina, isoladamente, aumentaram a densidade de receptores D1-sÃmile no corpo estriado enquanto que a atropina causou uma diminuiÃÃo dos receptores D2-sÃmile e uma upregulation dos receptores muscarÃnicos. O mazindol aumentou o binding de 3H-NMS no corpo estriado. O presente trabalho sugere, de maneira geral, que existe uma relaÃÃo entre os receptores muscarÃnicos M1 e M2 com os receptores dopaminÃrgicos D1 e D2, sendo que esta relaÃÃo pode ocorrer de maneira positiva ou negativa, dependendo da seletividade e da dose das drogas utilizadas
In the study, the interaction between the dopaminergic and cholinergic systems through the study of behavioral (open field and catalepsy) and neurochemical (density of dopaminergic receptor (D1 and D2-like) and muscarinic (M1+M2-like)) effect in striatum rat was evaluated. The following drugs were used: mazindol (indirect dopaminergic agonist), apomorphine (D1-like and D2-like dopaminergic agonist), pilocarpine (M1-like muscarnic aginist), carbachol (M-2like agonist muscarinc), pirenzepine (M1-like antagonist muscarinic), atropine (non-selective M1 and M2 antagonist muscarinic), clozapina(non-typical neuroleptic). The results showed that the pimozida and carbachol, alone or associated, caused increase in the cataleptic response and reduction in the motor activity. The mazindol also increased the motor activity. In small dosage, the carbachol and mazindol increased the density of D1-like receptors. Isolated, the pimozida and atropine increased the density of the D1-like receptors in striatum whereas the atropine caused a reduction of D2-like receptors and upregulation of muscarinic receptors. This work suggests a relationship, between muscarinc receptors M1 and M2 and dopaminergic receptors D1 and D2, and that this relationship can occur in a positive and negative manner, depending on the selectivity and the dose of the used drug
Tanimoto, Sonia Tomie. "\"Utilização da engenharia interfacial para a preparação de superfícies nano-estruturadas de Au pela aproximação bottom-up\"". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/75/75132/tde-11042007-105623/.
Pełny tekst źródłaThe subject of this work is focused in the utilization of a bottom-up approach to develop an Au nanostructured electrodeposits on the glassy carbon surface by a voltammetric procedure. These Au nanostructures have been characterized either by microscopic and voltammetric techniques. The critical dimensions of nanostructures has been evaluated by a Gausean normal data distribution curve and presented, as results a mean height of 35 nm and a mean diameter of 150 nm. The Au nanostructures were further modified by the deposition of a cystamine (thiol) self-assembled monolayer, yielding a suitable substrate for enzyme immobilization, as a possible future application. The electrochemical behaviour of dopamine and ascorbic acid on gold, Glassy Carbon and nanostructures was studied aiming to characterize the modified electrode. The 300 mV shift in the oxidation peak potential for ascorbic acid on gold in relation to Glassy Carbon allows to calculate the nanostructure coverage factor by the peak current inhibition as 43%. Finally, dopamine was employed to detect the self assembled monolayer formation on the Au nanostructure through its voltammetric behaviour. The variation in the oxidation potential for DA on gold and self assembled monolayer was used as an indicator for such modification.
Wu, Qun Garris Paul A. "Function and regulation of the dopamine transporter". Normal, Ill. Illinois State University, 1999. http://wwwlib.umi.com/cr/ilstu/fullcit?p9960430.
Pełny tekst źródłaTitle from title page screen, viewed July 31, 2006. Dissertation Committee: Paul A. Garris (chair), Maarten E.A. Reith, Anthony J. Otsuka, Robert L. Preston, David L. Williams. Includes bibliographical references (leaves 221-242) and abstract. Also available in print.
Marschinke, Franziska. "From dopamine nerve fiber formation to astrocytes". Doctoral thesis, Umeå : Department of Integrative Medical Biology, Section for Histology and Cell Biology, Umeå University, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-20615.
Pełny tekst źródłaJohnson, Nicholas. "Mechanistic insights into neuronal oscillatory activity in the dopamine-intact and dopamine-depleted primary motor cortex". Thesis, Aston University, 2017. http://publications.aston.ac.uk/30387/.
Pełny tekst źródłaKoshkina, Elena Hrebien Leonid. "Extracellular dopamine concentration control : computational model of feedback control /". Philadelphia, Pa. : Drexel University, 2006. http://hdl.handle.net/1860/1160.
Pełny tekst źródłaOmar, Muhammad Yusof. "Modulation of Presynaptic Dopamine Synthesis and Storage Dynamics by D2-Like Receptor Partial Agonist Antipsychotics in Rat Brain Striatum". Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670700.
Pełny tekst źródłaLa regulación dopaminérgica presináptica es importante para mantener un equilibrio homeostático de los niveles almacenados y liberación de dopamina. Los cambios en la neurotransmisión de dopamina contribuyen a los trastornos neurológicos y psiquiátricos. Hallazgos recientes de nuestro grupo (Ma et al., 2015; González-Sepúlveda et al., presentado) describieron los fuertes efectos de varias clases de medicamentos dopaminérgicos en la síntesis de dopamina, incluida L-DOPA (utilizada en Parkinson), tetrabenazina (Huntington) y aripiprazol (esquizofrenia). En este estudio, confirmamos y ampliamos esos hallazgos y comparamos los efectos de los antipsicóticos agonistas parciales D2R cariprazina y brexpiprazol, las psicoestimulantes anfetamina y metilfenidato varios otros compuestos selectivos y experimentales. El estriado cerebral de rata fue troceado e incubado ex-vivo en presencia o ausencia de estos fármacos a diferentes concentraciones. Espontáneamente, la dopamina y la serotonina se acumularon con el tiempo alcanzando niveles de almacenamiento casi máximos. Este enfoque experimental nos permitió evaluar su dinámica de síntesis y almacenamiento bajo la influencia de los agentes farmacológicos elegidos. Nuestros resultados podrían ser útiles para comprender los mecanismos de acción de los antipsicóticos, y podrían facilitar la investigación futura con modelos animales y ensayos clínicos utilizando nuevos agentes dopaminérgicos.
Presynaptic dopaminergic regulation is important to maintain a homeostatic balance of dopamine stored levels and release. Changes in dopamine neurotransmission contribute to neurological and psychiatric disorders. Recent findings from our group (Ma et al., 2015; González-Sepúlveda et al.,-submitted) describe strong effects of several classes of dopaminergic drugs on dopamine synthesis, including L-DOPA (used in Parkinson), tetrabenazine (Huntington) and aripiprazole (schizophrenia). In this study, I confirm and extend those findings and compare the effects of D2R partial agonist antipsychotics cariprazine and brexpiprazole, the psychostimulants amphetamine and methylphenidate, and several other selective and experimental compounds. Rat brain striatum was minced and incubated ex-vivo in the presence or absence of these drugs at different concentrations. Spontaneously, dopamine and serotonin accumulated over time reaching near-maximal storage levels. This experimental approach allowed me to evaluate their synthesis and storage dynamics under the influence of chosen pharmacological agents. My results could be useful to understand the mechanisms of action of antipsychotics, and they could facilitate further research with animal models and clinical trials using new dopaminergic agents.
Winter, Eduardo. "Influencia de compostos carboxilicos e ions metalicos na degradação de neurotransmissores". [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/249435.
Pełny tekst źródłaTese (doutorado) - Universidade Estadual de Campinas, Instituto de Quimica
Made available in DSpace on 2018-08-09T10:51:51Z (GMT). No. of bitstreams: 1 Winter_Eduardo_D.pdf: 3366512 bytes, checksum: 6c8baea3dd6502c19761ad449683bb95 (MD5) Previous issue date: 2007
Resumo: Muitas doenças neurodegenerativas são associadas com disfunções de neurotransmissores, em particular catecolaminas, no cérebro. Numerosas pesquisas têm indicado que íons metálicos podem induzir estresse oxidativo - dependente da neurodegeneração de dopamina e são responsáveis pelo aparecimento de doenças neurodegenerativas. Em estudos prévios foi verificado que alguns carboxilatos diminuem a velocidade de oxidação de catecolaminas e inibem a passivação de eletrodos sólidos durante a análise voltamétrica destes compostos fenólicos. Este trabalho teve por objetivo estudar a influência de carboxilatos (EDTA, NTA, EGTA, DTPA, acetato, citrato e oxalato) e íons metálicos (Ce(IV), Fe(III) e Hg(II)) durante a oxidação de neurotransmissores (dopamina, serotonina, epinefrina, norepinefrina e L-dopa) no intuito de estabelecer mecanismos de reações que possam contribuir no esclarecimento do papel destes compostos no processo de degeneração dos neurotransmissores, assim como compreender como os carboxilatos inibem o envenenamento do eletrodo durante a varredura de potencial. Para eses propósitos foram empregadas as técnicas de espectrofotometria, voltametria e espectroeletroquímica. A cela espectroeletroquímica de camada delgada desenvolvida incorporou um sistema de três eletrodos, sendo o eletrodo de trabalho uma minigrade de Pt. O sistema foi caracterizado usando o-tolidina e K4[Fe(CN)6]/ K3[Fe(CN)6] e permitiu o monitoramento das reações in situ. Os resultados obtidos mostraram que os carboxilatos desprotonados interagem com os produtos intermediários formados durante a oxidação das catecolaminas por meio de ligações de hidrogênio, sendo estas interações dependentes do pH do meio, estruturas do carboxilato e do próprio neurotransmissor. Foi proposto um mecanismo eletroquímico para a oxidação de aminas biogênicas na presença de carboxilatos no eletrodo de platina. A estabilização dos produtos intermediários formados inibe a formação de compostos poliméricos que são responsáveis pelo envenenamento do eletrodo. Do mesmo modo, os carboxilatos retardam ou inibem a oxidação química de algumas aminas biogênicas por íons metálicos
Abstract: Several neurological disorders are associated with improper catechoalmine regulation in the brain. Numerous researches have indicated that metallic ions can induce oxidative stress-dependent neurodegeneration of dopamine, and are responsible for the induction of neurodegenerative diseases. In previous work was verified that some carboxylates diminishes the oxidation rate of catecholamines and inhibit the well known solid state electrode passivation during voltammetric analysis of these phenolic compounds. The aim of this work was to study the influence of carboxylates (EDTA, NTA, EGTA, DTPA, acetate, oxalate and citrate) and metallic ions (Ce(IV), Fe(III) and Hg(II)) during the oxidation of neurotransmitters (dopamine, serotonin, epinephrine, norepinephrine and L-dopa) in order to establish putative reaction mechanism which could contribute to understand the role of these compounds in neurodegenerative processes, as well as comprehend how the carboxylates inhibit the electrode fouling during potential scan. For these purposes, the studies were carried out using spectrophotometric, voltammetric and spectroelectrochemical techniques. The spectroelectrochemical thin layer cell developed incorporated a three electrode system, using a Pt- minigrade as working electrode. The system was characterized employing o-tolidine and K4[Fe(CN)6]/ K3[Fe(CN)6] and allowed monitoring the electrode reactions in situ. The results obtained showed that the deprotonated carboxylates interacts with the intermediates formed at the electrochemical oxidation of catecholamines by hydrogen bonds. These interactions are dependent on the pH of the medium, as well as on the chemical structures of the carboxylates and neurotransmitters itself. An electrochemical mechanism for the oxidation of biogenic amines in the presence of carboxylates at the platinum electrode is proposed. The stabilization of the intermediates formed inhibits the formation of polymeric compounds that are responsible for the electrode fouling. In the same manner, the carbolxylates retards or inhibit the chemical oxidation of some biogenic amines by metallic ions by the same reaction pathway
Doutorado
Quimica Analitica
Doutor em Ciências
Middleton, Lisa Sue. "Nicotine receptor modulation of dopamine transporters". Lexington, Ky. : [University of Kentucky Libraries], 2005. http://lib.uky.edu/ETD/ukyphsc2006d00383/Middleton.pdf.
Pełny tekst źródłaTitle 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).
Laine, P. (Pekka). "Dopamine transporter in alcoholism:a SPET study". Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514265270.
Pełny tekst źródłaBlackburn, James Robert. "Involvement of dopamine in feeding behaviours". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25347.
Pełny tekst źródłaArts, Faculty of
Psychology, Department of
Graduate
Garside, Sarah. "Dopamine-glutamate interactions in the striatum". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq30137.pdf.
Pełny tekst źródłaSahai, Animesh. "Role of dopamine in diabetic nephropathy". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0023/NQ51665.pdf.
Pełny tekst źródłaKho, Tjioe Liang. "Dopamine and the circulation in man". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5365.
Pełny tekst źródłaHemdan, Sandy 1977. "Mechanisms of dopamine toxicity in oligodendrocytes". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115686.
Pełny tekst źródłaAddition of iron to cultures increased DA-induced expression of the stress protein heme oxygenase-1 (HO-1), and toxicity as assessed by mitochondrial activity, cellular release of lactate dehydrogenase, nuclear condensation and caspase-3 activation. In contrast, an iron chelator reduced these events. Furthermore, DA induced accumulation of superoxide, which was also reduced by the iron chelator. Surprisingly, a mimetic of the superoxide detoxifying enzyme, SOD potentiated DA toxicity, suggesting that generation of hydrogen peroxide via superoxide dismutation may be contributing to toxicity. Both a mimetic of the peroxide-scavenging enzyme, GPx and a GSH analog blocked DA-induced superoxide accumulation, HO-1 expression and caspase-3 activation. In addition, the GPx mimetic blocked caspase-3 activation induced by the combination of DA with iron. In contrast, an inhibitor of glutathione synthesis potentiated DA-induced HO-1 expression and cell death.
Finally, in further examining the cellular defense mechanisms, I found that various heat shock proteins increased in expression levels during oligodendroglial differentiation, however only heat shock protein-90 (HSP-90) was detected in oligodendrocyte progenitors. An HSP-90 inhibitor decreased activated Akt levels, induced caspase-3 activation, increased nuclear condensation, reduced oligodendrocyte progenitor viability, and potentiated DA-induced apoptosis. In addition, an Akt inhibitor alone exacerbated DA toxicity and in combination with the HSP-90 inhibitor caused synergistic potentiation of DA toxicity by enhancing caspase-3 activation.
In conclusion, elevated levels of iron, superoxide, deficient detoxification of peroxides by glutathione peroxidase and inadequate defense by glutathione contribute to the susceptibility of oligodendrocyte progenitors to DA-induced toxicity. On the other hand, HSP-90 alone or in concert with Akt play important roles in oligodendrocyte progenitors survival following an insult that produces oxidative stress.
Middleton, Lisa Sue. "NICOTINIC RECEPTOR MODULATION OF DOPAMINE TRANSPORTERS". UKnowledge, 2006. http://uknowledge.uky.edu/gradschool_diss/412.
Pełny tekst źródłaGenn, Rachel F. "Dopamine receptor subtypes and ingestive behaviour". Thesis, Durham University, 1999. http://etheses.dur.ac.uk/4303/.
Pełny tekst źródłaHilditch, A. "Pharmacological characterisation of peripheral dopamine receptors". Thesis, Open University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.352607.
Pełny tekst źródłaLefeuvre, Jocelyne. "Dépression, Dopamine et maladie de Parkinson". Bordeaux 2, 1991. http://www.theses.fr/1991BOR23034.
Pełny tekst źródłaBerry, Sally Ann. "The regulation of tuberoinfundibular dopamine neurons". Case Western Reserve University School of Graduate Studies / OhioLINK, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=case1054914406.
Pełny tekst źródłaGrogan, John Patrick. "Roles of dopamine in human memory". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.688105.
Pełny tekst źródłaHarper, Lucy V. "Renal dopamine and salt-retaining states". Thesis, Aston University, 2002. http://publications.aston.ac.uk/10948/.
Pełny tekst źródłaMuscat, Richard. "Behavioural microanalysis of dopamine autoreceptor function". Thesis, London Metropolitan University, 1987. http://repository.londonmet.ac.uk/3060/.
Pełny tekst źródłaCappellini, Rekha. "Dopamine and dopamine-quinones toxicity in Parkinson's disease: cellular models revealing a possible role for superoxide dismutases". Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423418.
Pełny tekst źródłaLa malattia di Parkinson è una diffusa sindrome neurodegenerativa che affligge circa il 2% della popolazione oltre l’età dei 60 anni. La caratteristica principale della patologia è la preferenziale morte dei neuroni dopaminergici della substantia nigra pars compacta del mesencefalo, e la presenza di inclusioni proteinacee chiamate Lewy body nei neuroni sopravvissuti. Nel 10% dei casi, la malattia è collegata a mutazioni su diversi geni, tra i quali α-synucleina, DJ-1, PARKIN, PINK1 e LRRK2, ma nella maggior parte dei casi (Parkinson sporadico) (Gwinn-Hardy 2002) l’eziologia è ancora sconosciuta. Da studi post mortem e da modelli in vitro e in vivo per il PD è stata rilevata una possibile connessione tra le forme genetiche e quelle sporadiche che implica sia la disfunzione mitocondriale e lo stress ossidativo come fattori centrali nella patogenesi della malattia (Gilgun-Sherki Y. et al. 2001, Mythri R. B. et al. 2011). Lo stress ossidativo è una condizione in cui le capacità antiossidanti della cellula non sono in grado di sopperire alla produzione di specie reattive dell’ossigeno (ROS). Questa condizione di sbilanciamento tra la produzione e la detossificazione dei ROS causa danni irreversibili ai componenti cellulari come lipidi, proteine e DNA, portando alla morte cellulare (Lotharius et al. 2002). Tra gli enzimi coinvolti nella difesa antiossidante delle cellule, le superossido dismutasi giocano un ruolo fondamentale poiché catalizzano la dismutazione dell’anione superossido in ossigeno molecolare e perossido di idrogeno (Fridovich 1995). Poiché lo stress ossidativo non spiega da solo la selettiva morte dei neuroni dopaminerigici, l’ipotesi è che la dopamina stessa abbia un ruolo chiave. In condizioni fisiologiche, la dopamina viene metabolizzata nel citosol e stoccata all’interno delle vescicole sinaptiche grazie all’azione del trasportatore vescicolare delle monoamine 2 (VMAT2) dove è stabilizzata dal basso pH (Erickson, J. D 1992). Se la concentrazione citosolica di dopamina supera quella fisiologica, essa viene metabolizzata ad acido 3,4-diidrofenilacetico e perossido di idrogeno grazie all’azione dell’enzima monoamina ossidasi (MAO) e aldeide deidrogenasi, o sequestrata nei lisosomi dove può auto ossidarsi a formare neuromelanina. Se non è metabolizzata in questi pathway, la dopamina può essere ossidata a dopamino-chinoni (DAQs) (spontaneamente o enzimaticamente) (Sulzer, D., 2000, Elsworth, J. D. 1997), una reazione che produce anche specie reattive dell’ossigeno (ROS). Con queste premesse, abbiamo valutato due linee di ricerca usando un modello in vitro per il PD (la linea cellulare SH SY5Y): la prima riguardante l’effetto della dopamina e le sue forme di ossidazione sulla vitalità cellulare, la seconda sul potenziale ruolo dell’over espressione delle superossido dismutasi (1 e 2). Utilizzando differenti tecniche abbiamo iniziato a valutare quale pathway di morte cellulare veniva attivato dalla dopamina e dalle sue forme ossidate. Andando a valutare la frammentazione nucleare, uno degli ultimi stadi dell’apoptosi, abbiamo determinato che sia la dopamina sia i chinoni inducono l’attivazione di questo processo di morte. Per confermare il processo apoptotico, abbiamo valutato un altro marker: l’esternalizzazione delle fosfatidil-serine (PS): uno dei primi stadi di attivazione del processo apoptotico. con l’utilizzo di ANNEXIN-V-FLUOS, una sonda specifica per le PS. Mediante la tecnica di citoflurimetria abbiamo confermato che sia la dopamina che i chinoni attivano l’apoptosi. Successivamente abbiamo voluto valutare se la dopamina e i chinoni avevano effetti tossici a livello extracellulare o necessitavano di entrare nelle cellule. Pre-trattando le cellule con l’inibitore specifico del trasportatore della dopamina (GBR 12909) abbiamo dimostrato che la tossicità della dopamina è dipendente dal suo trasporto all’interno della cellula (in quanto il trattamento con l’inibitore ha avuto un effetto protettivo per le cellule), mentre i chinoni non lo necessitano. Poichè lo stress ossidativo è stato proposto come possibile meccanismo implicato nella patogenesi della malattia, e la chimica ossidativa della dopamina (auto ossidazione e ossidazione mediata da enzimi) porta alla produzione di specie radicaliche, abbiamo valutato la produzione dell’anione superossido (la prima specie radicalica prodotta soprattutto a livello del mitocondrio) usando una sonda specifica. I dati dimostrano che solo il processo auto ossidativo della dopamina porta alla produzione di anione superossido e che questo processo è dipendente dall’internalizzazione della dopamina a livello del trasportatore. Per comprendere maggiormente il meccanismo alla base della tossicità del processo di ossidazione e ossidazione mediate da enzima della dopamina abbiamo valutato altri marker di apoptosi. Poiché dai dati precedenti è stato visto che solo la dopamina citosolica era in grado di indurre la produzione dell’anione superossido a livello del mitocondrio, abbiamo voluto verificare se i due processi ossidativi della dopamina, attivassero differenti pathway apoptotici (i prevalenti comprendo la via mediata dai recettori di morte, l’altro quella mitocondriale). Dati preliminari dimostrano una marcata attivazione della caspasi 3 e la conseguente inattivazione della poli (ADP) ribosio polimerasi in conseguenza al trattamento con i chinoni suggerendoci di investigare maggiormente sulle possibili differenze tra i diversi processi ossidativi della dopamina. La seconda parte del progetto si è focalizzata sul possibile ruolo delle superossido dismutasi 1 e 2 contro la tossicità indotta dalla dopamina e dai suoi prodotti di ossidazione. L’over espressione sia della SOD1 che della SOD2 hanno rivelato un effetto protettivo contro la produzione di anione superossido indotto dalla dopamina, mentre non hanno presentato alcun effetto contro la tossicità indotta dai chinoni rimarcando il ruolo dell’anione superossido nella tossicità indotta dalla dopamina. Nel presente progetto di dottorato, abbiamo valutato l’ipotesi che lo stress ossidativo indotto dalla dopamina e dalle sue specie ossidate possa avere un ruolo chiave nella specifica degenerazione dei neuroni dopaminergici caratteristici della malattia di Parkinson. I dati ottenuti sembrano dare indicazioni sulla differente attivazione di pathway di morte cellulare indotta dalla dopamina e dalle sue forme ossidate con un differente ruolo nella produzione dell’anione superossido. Poichè lo stress ossidativo è considerate uno dei meccanismi che collegano il Parkinson sporadico a quello genetico e la dopamina, nella sua chimica ossidativa, porta alla produzione di specie radicaliche, riuscire a capire quale pathway di morte cellulare è attivato e in quale misura, è cruciale per lo sviluppo di terapie per impedire l’inizio e la progressione della malattia. I dati derivanti dall’over espressione delle superossido dismutasi dimostrano che composti che impediscono la formazione dell’anione superossido (come SOD-mimetici che sono attualmente usati per altre patologie) potrebbero avere un ruolo protettivo contro lo stress ossidativo e la conseguente morte cellulare indotta. Inoltre, anche composti in grado ci bloccare la cascata apoptotica indotta da dopamina e chinoni potrebbe proteggere dalla morte le cellule affette in questa malattia neurodegenerativa
Avalos, Melva Nidia. "Partial agonist interactions with dopamine in clonal cell lines expressing recombinant receptors : towards a molecular model of antipsychotic drug action /". Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.
Pełny tekst źródłaKanbertay, Elif. "Synthesis Of Dopamine Functionalized Silver Nanoparticles Together With Possible Interactions Between Silver And Dopamine Having Different Oxidation Forms". Master's thesis, METU, 2013. http://etd.lib.metu.edu.tr/upload/12615658/index.pdf.
Pełny tekst źródłaAl-Ali, Asmaa M. H. "Understanding the role of dopamine D4 receptor regulation of mesolimbic dopamine function in a rat model of schizophrenia". Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/43047.
Pełny tekst źródłaMariani, Louise-Laure. "Biosensor imaging of dopamine and glutamate signaling in striatal projection neurons in a mouse model of dopamine depletion". Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS511.
Pełny tekst źródłaParkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease. There is currently no cure for PD. Symptomatic drug therapy essentially relies on dopamine (DA) replacement therapy. The spectacular antiparkinsonian effect of levodopa in PD is however hampered by long-term complications, motor fluctuations and dyskinesia in all patients at some time during the disease course. The mechanisms of the maladaptive striatal plasticity leading to dyskinesia are not well understood. The aim of this project was to identify the dysregulations of signaling pathways in striatal projection neurons (SPN) in the absence of dopamine. We used a mouse model of lesion of DA neurons with 6-OHDA and virally transduced biosensors to monitor signaling pathways in live neurons with two-photon imaging of corticostriatal slices. We focused our attention on extracellular signal-regulated kinase (ERK), cAMP-dependent protein kinase (PKA) and Ca2+ which are known to be altered in the absence of DA. We first set up a reliable experimental model in adult mice, successfully combining 6-OHDA and viral vector in the same unilateral stereotactic injection into the dorsal striatum. In some experiments we targeted the biosensor expression to specific neuronal populations using Cre-dependent “flexed” biosensors. We used mice expressing Cre under the control of the D1 DA receptor (D1R) promoter to target specifically striatal projection neurons of the direct pathway (dSPNs) or the adenosine A2A receptor (A2AR) to target SPNs of the indirect pathway (iSPNs). We used fluorescence resonance energy transfer (FRET)-based biosensors EKAR-EV and AKAR-3 to monitor ERK and PKA activities, respectively. We also monitored cytosolic free Ca2+ with the genetically encoded calcium indicator GCaMP6S. We used pharmacological tools to modulate glutamate, DA, and adenosine receptors as well as phosphodiesterases (PDE) and kinases activities. We observed that the DA lesion increased ERK responsiveness to stimulation of D1R. Since ERK activation depends on both cAMP and Ca2+ signals, we then investigated these two pathways. We observed an increased activation of PKA in response to D1R but not A2AR. We explored the mechanism of this increased sensitivity using mice deficient for Gαolf, the G protein that couples striatal receptors to adenylyl cyclase. We provided evidence that increased levels of Gαolf contributed to enhanced D1 responses after 6-OHDA lesions and identified a deficit in PDE activity in D1 neurons that was likely to amplify this effect. By monitoring Ca2+ signals we showed an increased spontaneous activity of D1 neurons in lesioned mice. However, unexpectedly the Ca2+ responses to stimulation of AMPA glutamate receptors were increased in iSPNs and not dSPNs. In conclusion, our work using for the first time 2-photon biosensor imaging in the DA-depleted striatum of adult mice confirms and extends previous observations on signaling dysregulations in the absence of DA. It reveals distinct cell type-specific alterations of cAMP, Ca2+ and ERK responses in the two populations of SPNs and suggests possible mechanisms for these alterations
Jaworski, Jason Noel. "Effect of dopamine D2/D3 receptor antagonist sulpiride on changes in mesolimbic dopamine produced by amphetamine and ethanol /". Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3008360.
Pełny tekst źródłaHeusner, Carrie L. "Genetic analysis of striatal glutamate-dopamine interactions /". Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/9212.
Pełny tekst źródłaEvans, Anthony Mark. "Dopamine receptors of the cockroach salivary gland". Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/27986.
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