Spelling suggestions: "subject:"dopamine"" "subject:"d'opamine""
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Comparison of the Role of Dopamine in Egocentric and Allocentric Learning, Two Subtypes of NavigationBraun, Amanda Ann 11 September 2015 (has links)
No description available.
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A Computational Analysis of Dopamine Signaling at the Level of the Varicosity in Rodent StriatumRooney, Katherine Elizabeth January 2015 (has links)
No description available.
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Effect of age on dopamine receptor function and the action of nialamide in the nucleus accumbens of rats /Cousin, Kelley Martin January 1985 (has links)
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Studies on the adrenergic and dopaminergic activities of sulfur-containing catecholamine analogs /Ross, Phillip Cole January 1986 (has links)
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Part 1: Synthesis of irreversible inhibitors of Aldose reductase with subsequent development of carbon-13 NMR protein probe. Part 2: Synthesis of selenium analogs of dopamine as potential dopamine receptor agonists /Ares, Jeffrey Joseph January 1986 (has links)
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Perturbations de la transmission dopaminergique chez les souris présentant une réduction de nurr1Baillargeon, Joanie 13 April 2018 (has links)
Le facteur de transcription Nurrl est un récepteur nucléaire orphelin hautement impliqué dans le développement du système dopaminergique. Son expression persistante à l'âge adulte soulève toutefois de nombreuses questions quant à son rôle exact dans le cerveau mature. L'objectif de cette étude était d'évaluer les effets d'une diminution partielle du facteur de transcription Nurrl sur la transmission dopaminergique chez des souris adultes. Nous avons d'abord observé qu'une réduction partielle de Nurrl n'influence pas le comportement locomoteur des souris en conditions basales. Par contre, l'administration aiguë d'amphétamine chez les souris Nurrl (+/-) induit une brève augmentation de l'activité locomotrice précédant l'apparition marquée de mouvements verticaux et stéréotypés. La modulation de différents marqueurs tels que Nurrl, Nur77, Nor-1 et l'ENK fut également étudiée. De façon générale, nos résultats démontrent des modifications plus ou moins importantes de l'expression de ce neuropeptide et de ces récepteurs nucléaires en présence ou non du psychostimulant. Enfin, l'ensemble de ces résultats suggèrent qu'une réduction partielle de Nurrl induit des changements importants dans la transmission dopaminergique
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Interventions pharmacologiques affectants spécifiquement la signalisation du récepteur D2 de la dopamine médiée par la beta arrestine 2Fakhfouri, Gohar 01 February 2021 (has links)
No description available.
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Cocaine Use Modulates Neural Prediction Error During Aversive LearningWang, John Mujia 08 June 2015 (has links)
Cocaine use has contributed to 5 million individuals falling into the cycle of addiction. Prior research in cocaine dependence mainly focused on rewards. Losses also play a critical role in cocaine dependence as dependent individuals fail to avoid social, health, and economic losses even when they acknowledge them. However, dependent individuals are extremely adept at escaping negative states like withdrawal. To further understand whether cocaine use may contribute to dysfunctions in aversive learning, this paper uses fMRI and an aversive learning task to examine cocaine dependent individuals abstinent from cocaine use (C-) and using as usual (C+). Specifically of interest is the neural signal representing actual loss compared to the expected loss, better known as prediction error (δ), which individuals use to update future expectations. When abstinent (C-), dependent individuals exhibited higher positive prediction error (δ+) signal in their striatum than when they were using as usual. Furthermore, their striatal δ+ signal enhancements from drug abstinence were predicted by higher positive learning rate (α+) enhancements. However, no relationships were found between drug abstinence enhancements to negative learning rates (α±-) and negative prediction error (δ-) striatal signals. Abstinent (C-) individuals' striatal δ+ signal was predicted by longer drug use history, signifying possible relief learning adaptations with time. Lastly, craving measures, especially the desire to use cocaine and positive effects of cocaine, also positively correlated with C- individuals' striatal δ+ signal. This suggests possible relief learning adaptations in response to higher craving and withdrawal symptoms. Taken together, enhanced striatal δ+ signal when abstinent and adaptations in relief learning provide evidence in supporting dependent individuals' lack of aversive learning ability while using as usual and enhanced relief learning ability for the purpose of avoiding negative situations such as withdrawal, suggesting a neurocomputational mechanism that pushes the dependent individual to maintains dependence. / Master of Science
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The role of the μ-opioid receptors in the mechanism of ethanol-stimulated mesolimbic dopamine releaseJob, Martin Olufemi 05 February 2010 (has links)
The goal of this dissertation was to investigate the role of μ-opioid receptors in
the mechanism of ethanol-stimulated dopamine release in the nucleus
accumbens shell (NAcS) of rats. The underlying hypothesis is that blockade of
the μ-opioid receptors leads to an attenuation of ethanol-stimulated mesolimbic
dopamine release. We prepared ethanol-naïve male Long Evans rats (n = 95) for
intravenous (i.v.) drug administration and in vivo microdialysis (in awake, freely
moving animals), and analyzed our samples using HPLC and GC for dopamine
and ethanol detection, respectively. In one set of experiments, we looked at the
effects of naltrexone, a non-selective opioid antagonist, on ethanol-stimulated
mesolimbic dopamine release. First of all, we checked to see if naltrexone
affected basal dopamine levels in the NAcS. Thereafter, we looked for a dose of
naltrexone (i.v.) that was effective in suppressing the release of dopamine in the
NAcS evoked by morphine (1 mg/kg, i.v.). Subsequently, we checked to see if
doses of naltrexone that inhibited morphine-evoked dopamine were also effective in attenuating dopamine release due to ethanol (1g/kg, 10% w/v, i.v.). To do this,
we pretreated rats with naltrexone doses, followed 20 min later by morphine,
ethanol or saline (all drugs were administered i.v.). In another set of experiments,
we looked at the effect of β-funaltrexamine, a selective μ-opioid antagonist, on
ethanol-stimulated dopamine release in the NAcS. Similarly to the previous set of
experiments, we looked for a dose of β-funaltrexamine (s.c.) that was effective in
suppressing the release of dopamine the NAcS evoked by morphine (1 mg/kg,
i.v.), and checked to see if this dose of β-funaltrexamine was also effective in
attenuating ethanol-stimulated dopamine release in the NAcS. For the β-
funaltrexamine experiments, rats were pretreated with β-funaltrexamine (s.c.) 20-
25 h before i.v. infusions of saline, morphine and ethanol.
Morphine increased dopamine release in the NAcS. Naltrexone and β-
funaltrexamine significantly attenuated morphine-evoked dopamine release.
Also, ethanol increased dopamine release in the NAcS. Naltrexone and β-
funaltrexamine, at doses effective in attenuating morphine-evoked dopamine
release, suppressed the prolongation, but not the initiation of dopamine release
in the NAcS due to ethanol. Naltrexone and β-funaltrexamine did not affect the
peak concentration and clearance of ethanol in the brain. The conclusion of this
study is that the μ-opioid receptors are involved in a delayed component of
ethanol-stimulated dopamine release in the NAcS in ethanol-naïve rats. This is
the first study to show that the ethanol-stimulated dopamine response consists of
a delayed μ-opioid mechanism. / text
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Brain Signaling Mechanisms Through Which Dopamine Stimulates Maternal Behavior in RatsZhang, Ke-You January 2008 (has links)
Thesis advisor: Michael Numan / This paper will review research from our laboratory dealing with the neural basis of maternal behavior in rats. Specifically, my work investigates hypothalamic interaction with the mesolimbic dopamine system and the regulation of maternal responsiveness. Recent evidence has shown that increased dopamine activity in the nucleus accumbens, a major terminus of the mesolimbic dopamine pathway, results in a facilitation of maternal behavior in female rats who have been partially primed by hormones. However, the way in which dopamine and hormones act on these neural circuits is unclear. We hypothesize that one of these hormones, estradiol, acts on the MPOA and mesolimbic dopamine system through similar intracellular mechanisms as dopamine. My research goals are twofold: (1) to discern which G-protein coupled pathway dopamine utilizes to act in the nucleus accumbens and (2) to investigate whether estradiol is having rapid effects at the cell membrane and whether these effects are mediated by G-protein coupled receptors. / Thesis (BA) — Boston College, 2008. / Submitted to: Boston College. College of Arts and Sciences. / Discipline: Psychology. / Discipline: College Honors Program.
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