Gotowe bibliografie tematyczne / Dopamine

Gotowa bibliografia na temat „Dopamine”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 7 września 2024

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Artykuły w czasopismach na temat "Dopamine"

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Helms, My N., Xi-Juan Chen, Semra Ramosevac, Douglas C. Eaton i Lucky Jain. "Dopamine regulation of amiloride-sensitive sodium channels in lung cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 290, nr 4 (kwiecień 2006): L710—L722. http://dx.doi.org/10.1152/ajplung.00486.2004.

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Dopamine increases lung fluid clearance. This is partly due to activation of basolateral Na-K-ATPase. However, activation of Na-K-ATPase by itself is unlikely to produce large changes in transepithelial transport. Therefore, we examined apical and basolateral dopamine's effect on apical, highly selective sodium channels [epithelial sodium channels (ENaC)] in monolayers of an alveolar type 2 cell line (L2). Dopamine increased channel open probability ( Po) without changing the unitary current. The D1 receptor blocker SCH-23390 blocked the dopamine effect, but the D2 receptor blocker sulpiride did not. The dopamine-mediated increase in ENaC activity was not a secondary effect of dopamine stimulation of Na-K-ATPase, since ouabain applied to the basolateral surface to block the activity of Na-K-ATPase did not alter dopamine-mediated ENaC activity. Protein kinase A (PKA) was not responsible for dopamine's effect since a PKA inhibitor, H89, did not reduce dopamine's effect. However, cpt-2-O-Me-cAMP, which selectively binds and activates EPAC (exchange protein activated by cAMP) but not PKA, increased ENaC Po. An Src inhibitor, PP2, and the phosphatidylinositol-3-kinase inhibitor, LY-294002, blocked dopamine's effect on ENaC. In addition, an MEK blocker, U0126, an inhibitor of phospholipase A2, and a protein phosphatase inhibitor also blocked the effect of dopamine on ENaC Po. Finally, since the cAMP-EPAC-Rap1 pathway also activates DARPP32 (32-kDa dopamine response protein phosphatase), we confirmed that dopamine phosphorylates DARPP32, and okadaic acid, which blocks phosphatases (DARPP32), also blocks dopamine's effect. In summary, dopamine increases ENaC activity by a cAMP-mediated alternative signaling pathway involving EPAC and Rap1, signaling molecules usually associated with growth-factor-activated receptors.
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DeFrance, J. F., R. W. Sikes i R. B. Chronister. "Dopamine action in the nucleus accumbens". Journal of Neurophysiology 54, nr 6 (1.12.1985): 1568–77. http://dx.doi.org/10.1152/jn.1985.54.6.1568.

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The action of dopamine was studied in the nucleus accumbens of acutely prepared rabbits. Dopamine was applied iontophoretically to those cells and cell populations that responded in a monosynaptic excitatory manner to ipsilateral fimbrial stimulation. This strategy was adopted to isolate the effects of dopamine on postsynaptic receptors thus avoiding the bias resulting from activation of presynaptic dopamine receptors on dopaminergic afferents. Dopamine was found to have a suppressive effect on the excitatory (N) component of the field response and on driven extracellular unitary discharges. The specificity of dopamine's effect with receptors was indicated by the facts that fluphenazine effectively antagonized dopamine's effect, whereas bicuculline did not. The effect of dopamine was dependent on the rate of fimbrial stimulation. Dopamine has a marked suppressive effect on the fimbria-induced response at 0.5 Hz of stimulation but not at 6.0 Hz. This frequency specificity could not be linked directly to a cyclic adenosine 3',5'-cyclic monophosphate (cyclic AMP) mechanism because the iontophoresis cyclic AMP and dibutyryl cyclic AMP had suppressive effects at both 0.5 and 6.0 Hz rates of stimulation. It is suggested that dopamine acts in the nucleus accumbens to increase the "signal-to-noise" ratio. This might be a form of "contrast enhancement" of an incoming hippocampal message.
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Shin, Seon H., Samia F. Hanna, Murray Hong i Khem Jhamandas. "Reexamination of dopamine as the prolactin-release inhibiting factor (PIF): supplementary agent may be required for dopamine to function as the physiological PIF". Canadian Journal of Physiology and Pharmacology 68, nr 9 (1.09.1990): 1226–30. http://dx.doi.org/10.1139/y90-184.

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A large number of studies have been performed concerning dopamine's inhibitory effect on prolactin release, but many of these studies have examined the effect of dopamine dissolved in a solution containing ascorbic acid. Ascorbic acid, routinely used to protect dopamine from oxidation, alone does not stimulate or inhibit prolactin release, but it can potentiate the inhibitory effect of dopamine in a static monolayer culture system by approximately 100 times. We have closely examined the inhibitory effect of dopamine on prolactin release in the absence of ascorbic acid using a perifusion system. Male rat adenohypophyses were dispersed with trypsin and cultured in a Petri dish to form cell clusters. Inhibition of prolactin release by dopamine (1 μmol/L) in the absence of ascorbic acid was sustained for only 63 min during the 2-h perifusion period. Following a 2-h period of incubation of dopamine in the same experimental solution, the dopamine concentration was reduced from 1 to 0.18 μmol/L, yet this "2-h-old dopamine" was still effective in inhibiting prolactin release (approximately 30 min). This result suggests that the lactotrophs may be desensitized by chronic exposure to a high concentration of dopamine in the absence of ascorbic acid. In contrast, when a low concentration of dopamine (3 nmol/L) containing ascorbic acid (0.1 mmol/L) was perifused, inhibition of prolactin release was sustained for the entire 2-h perifusion period. Although there may be a large number of explanations for dopamine's transient inhibitory effect on prolactin release, the present results suggest that dopamine may require supplementary agent(s) to effectively inhibit prolactin release and thus function as the prolactin release inhibitory factor (PIF). We propose ascorbic acid as a major candidate for the supplementary factor for the PIF.Key words: dopamine, somatostatin, prolactin, cell cluster, perifusion.
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Macedo-Lima, Matheus, i Luke Remage-Healey. "Dopamine Modulation of Motor and Sensory Cortical Plasticity among Vertebrates". Integrative and Comparative Biology 61, nr 1 (3.04.2021): 316–36. http://dx.doi.org/10.1093/icb/icab019.

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Synopsis Goal-directed learning is a key contributor to evolutionary fitness in animals. The neural mechanisms that mediate learning often involve the neuromodulator dopamine. In higher order cortical regions, most of what is known about dopamine’s role is derived from brain regions involved in motivation and decision-making, while significantly less is known about dopamine’s potential role in motor and/or sensory brain regions to guide performance. Research on rodents and primates represents over 95% of publications in the field, while little beyond basic anatomy is known in other vertebrate groups. This significantly limits our general understanding of how dopamine signaling systems have evolved as organisms adapt to their environments. This review takes a pan-vertebrate view of the literature on the role of dopamine in motor/sensory cortical regions, highlighting, when available, research on non-mammalian vertebrates. We provide a broad perspective on dopamine function and emphasize that dopamine-induced plasticity mechanisms are widespread across all cortical systems and associated with motor and sensory adaptations. The available evidence illustrates that there is a strong anatomical basis—dopamine fibers and receptor distributions—to hypothesize that pallial dopamine effects are widespread among vertebrates. Continued research progress in non-mammalian species will be crucial to further our understanding of how the dopamine system evolved to shape the diverse array of brain structures and behaviors among the vertebrate lineage.
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Price, Christopher J., i Quentin J. Pittman. "Dopamine D4 Receptor Activation Inhibits Presynaptically Glutamatergic Neurotransmission in the Rat Supraoptic Nucleus". Journal of Neurophysiology 86, nr 3 (1.09.2001): 1149–55. http://dx.doi.org/10.1152/jn.2001.86.3.1149.

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Oxytocin and vasopressin release from magnocellular neurons of the supraoptic nucleus is under the control of glutamate-dependent excitation. The supraoptic nucleus also receives a generalized dopaminergic input from hypothalamic sources. To determine if dopamine can influence this excitatory drive onto the magnocellular neurons, we used whole-cell patch clamp to record the effect of dopamine on evoked and miniature excitatory postsynaptic currents in rat hypothalamic slices. Dopamine exposure (30 μM to 1 mM) induced a large and reversible reduction in the amplitude of evoked excitatory postsynaptic current in nearly all magnocellular cells tested. D4 receptors appeared to mediate dopamine's activity, based on inhibition of the response with 50 μM clozapine, but not by SCH 23390 or sulpiride, and mimicry of dopamine's action with the D4 specific agonist, PD 168077. Analysis of paired-pulse experiments and miniature postsynaptic currents indicated that dopamine's action involved a presynaptic mechanism, since the frequency of miniature postsynaptic currents was reduced with dopamine exposure without any change in current kinetics or amplitude, while the paired-pulse ratio increased. We therefore have demonstrated for the first time a role for dopamine D4 receptors in the supraoptic nucleus in the presynaptic inhibition of glutamatergic neurotransmission onto magnocellular neurons.
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Shull, Timothy E., Jasmina Kurepa i Jan A. Smalle. "Dopamine Inhibits Arabidopsis Growth through Increased Oxidative Stress and Auxin Activity". Stresses 3, nr 1 (2.03.2023): 351–71. http://dx.doi.org/10.3390/stresses3010026.

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Like some bacterial species and all animals, plants synthesize dopamine and react to its exogenous applications. Despite dopamine’s widespread presence and activity in plants, its role in plant physiology is still poorly understood. Using targeted experimentation informed by the transcriptomic response to dopamine exposure, we identify three major effects of dopamine. First, we show that dopamine causes hypersensitivity to auxin indole-3-acetic acid by enhancing auxin activity. Second, we show that dopamine increases oxidative stress, which can be mitigated with glutathione. Third, we find that dopamine downregulates iron uptake mechanisms, leading to a decreased iron content—a response possibly aimed at reducing DA-induced oxidative stress. Finally, we show that dopamine-induced auxin sensitivity is downstream of glutathione biosynthesis, indicating that the auxin response is likely a consequence of DA-induced oxidative stress. Collectively, our results show that exogenous dopamine increases oxidative stress, which inhibits growth both directly and indirectly by promoting glutathione-biosynthesis-dependent auxin hypersensitivity.
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Pfeiffer-Linn, C., i E. M. Lasater. "Dopamine modulates in a differential fashion T- and L-type calcium currents in bass retinal horizontal cells." Journal of General Physiology 102, nr 2 (1.08.1993): 277–94. http://dx.doi.org/10.1085/jgp.102.2.277.

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White bass (Roccus chrysops) retinal horizontal cells possess two types of voltage-activated calcium currents which have recently been characterized with regard to their voltage dependence and pharmacology (Sullivan, J., and E. M. Lasater. 1992. Journal of General Physiology. 99:85-107). A low voltage-activated transient current was identified which resembles the T-type calcium current described in a number of other preparations, along with a sustained high threshold, long-lasting calcium current that resembles the L-type calcium current. Here we report on the modulation of horizontal cell calcium channels by dopamine. Under whole-cell voltage clamp conditions favoring the expression of both calcium currents, dopamine had opposing actions on the two types of voltage-sensitive calcium currents in the same cone-type horizontal cell. The L-type calcium current was significantly potentiated by dopamine while the T-type current was simultaneously reduced. Dopamine had no effect on calcium currents in rod-type horizontal cells. Both of dopamine's actions were mimicked with the D1 receptor agonist, SKF 38393, and blocked by application of the D1 specific antagonist, SCH 23390. Dopamine's actions on the two types of calcium currents in white bass horizontal cells are mimicked by the cell membrane-permeant cyclic AMP derivative, 8-(4-chlorophenylthio)-cyclic AMP, suggesting that dopamine's action is linked to a cAMP-mediated second messenger system. Furthermore, the inhibitor of cAMP-dependent protein kinase blocked both of dopamine's actions on the voltage-dependent calcium channels when introduced through the patch pipette. This indicates that protein phosphorylation is involved in modulating horizontal cell calcium channels by dopamine. Taken together, these results show that dopamine has differential effects on the voltage-dependent calcium currents in retinal horizontal cells. The modulation of these currents may play a role in shaping the response properties of horizontal cells.
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Kundu, Aman, i Gyanesh Singh. "Dopamine synergizes with caffeine to increase the heart rate of Daphnia". F1000Research 7 (1.03.2018): 254. http://dx.doi.org/10.12688/f1000research.12180.1.

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Dopamine is a key neurotransmitter, and is widely used as a central nervous system (CNS) agent. Dopamine plays an important role in humans, including a major role in reward and motivation behaviour. Several addictive drugs are well known to increase neuronal dopamine activity. We selected Daphnia, an important model organism, to investigate the effect(s) of selected CNS agents on heart rate. Dopamine’s effects on Daphnia’s heart has not been previously reported. Caffeine is a well-known and widely consumed stimulant. Ethanol is well known for its effects on both neurological and physiological processes in mammals. We tested the effect of dopamine on the heart rate of Daphnia, and compared its effect with caffeine and ethanol alone and in combination. Both caffeine and dopamine were found to instantly increase the heart rate of Daphnia in a dose-dependent manner. Interestingly, caffeine synergized with dopamine to increase Daphnia’s heart rate. As ethanol decreased the heart rate of Daphnia and dopamine increased the heart rate of Daphnia, we wanted to test the effect of these molecules in combination. Indeed, Dopamine was able to restore the ethanol-induced decrease in the heart rate of Daphnia. Effects of these CNS agents on Daphnia can possibly be correlated with similar effects in the case of mammals.
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Sarkar, D. K., K. Chaturvedi, S. Oomizu, N. I. Boyadjieva i C. P. Chen. "Dopamine, Dopamine D2 Receptor Short Isoform, Transforming Growth Factor (TGF)-β1, and TGF-β Type II Receptor Interact to Inhibit the Growth of Pituitary Lactotropes". Endocrinology 146, nr 10 (1.10.2005): 4179–88. http://dx.doi.org/10.1210/en.2005-0430.

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The neurotransmitter dopamine is known to inhibit prolactin secretion and the proliferation of lactotropes in the pituitary gland. In this study, we determined whether dopamine and TGFβ1 interact to regulate lactotropic cell proliferation. We found that dopamine and the dopamine agonist bromocriptine stimulated TGFβ1 secretion and TGFβ1 mRNA expression but inhibited lactotropic cell proliferation both in vivo and in vitro. The dopamine’s inhibitory action on lactotropic cell proliferation was blocked by a TGFβ1-neutralizing antibody. We also found that PR1 cells, which express low amounts of the dopamine D2 receptor, demonstrated reduced expression of TGFβ1 type II receptor and TGFβ1 mRNA levels and had undetectable levels of TGFβ1 protein. These cells showed a reduced TGFβ1 growth-inhibitory response. Constitutive expression of the D2 receptor short isoform, but not the D2 receptor long isoform, induced TGFβ1 and TGFβ1 type II receptor gene expression and recovered dopamine- and TGFβ1-induced growth inhibition in PR1 cells. The constitutive expression of D2 receptor short isoform also reduced the tumor cell growth rate. These data suggest that a TGFβ1 system may mediate, in part, the growth-inhibitory action of dopamine on lactotropes.
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Ryczko, Dimitri, Jackson J. Cone, Michael H. Alpert, Laurent Goetz, François Auclair, Catherine Dubé, Martin Parent, Mitchell F. Roitman, Simon Alford i Réjean Dubuc. "A descending dopamine pathway conserved from basal vertebrates to mammals". Proceedings of the National Academy of Sciences 113, nr 17 (11.04.2016): E2440—E2449. http://dx.doi.org/10.1073/pnas.1600684113.

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Dopamine neurons are classically known to modulate locomotion indirectly through ascending projections to the basal ganglia that project down to brainstem locomotor networks. Their loss in Parkinson’s disease is devastating. In lampreys, we recently showed that brainstem networks also receive direct descending dopaminergic inputs that potentiate locomotor output. Here, we provide evidence that this descending dopaminergic pathway is conserved to higher vertebrates, including mammals. In salamanders, dopamine neurons projecting to the striatum or brainstem locomotor networks were partly intermingled. Stimulation of the dopaminergic region evoked dopamine release in brainstem locomotor networks and concurrent reticulospinal activity. In rats, some dopamine neurons projecting to the striatum also innervated the pedunculopontine nucleus, a known locomotor center, and stimulation of the dopaminergic region evoked pedunculopontine dopamine release in vivo. Finally, we found dopaminergic fibers in the human pedunculopontine nucleus. The conservation of a descending dopaminergic pathway across vertebrates warrants re-evaluating dopamine’s role in locomotion.
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Rozprawy doktorskie na temat "Dopamine"

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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.

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Neuro-computational models allow to study the brain mechanisms involved in intelligent behavior and extract essential computational principles which can be implemented in cognitive systems. They are a promising solution to achieve a brain-like artificial intelligence that can compete with natural intelligence on realistic behaviors. A crucial property of intelligent behavior is motivation, defined as the incentive to interact with the world in order to achieve specific goals, either extrinsic (obtaining rewards such as food or money, or avoiding pain) or intrinsic (satisfying one’s curiosity, fun). In the human brain, motivated or goal-directed behavior depends on a network of different structures, including the prefrontal cortex, the basal ganglia and the limbic system. Dopamine, a neurotransmitter associated with reward processing, plays a central role in coordinating the activity of this network. It structures processing in high-level cognitive areas along a limbic-associative-motor gradient and impacts the learning capabilities of the whole system. In this habilitation thesis, I present biologically-constrained neuro-computational models which investigate the role of dopamine in visual object categorization and memory retrieval (Vitay and Hamker, 2008), reinforcement learning and action selection (Vitay and Hamker, 2010), the updating, learning and maintenance of working memory (Schroll et al., 2012) and timing processes (Vitay and Hamker, 2014). These models outline the many mechanisms by which the dopaminergic system regulates cognitive and emotional behavior: bistable processing modes in the cerebral cortex, modulation of synaptic transmission and plasticity, allocation of cognitive resources and signaling of relevant events. Finally, I present a neural simulator able to simulate a variety of neuro-computational models efficiently on parallel architectures (Vitay et al., 2015)
Neuronale 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)
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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.

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The primary focus of the present thesis is the exploration of factors that influence the dopamine (DA) neuron by examining the expression of the dopamine transporter (DAT), a marker of the DA neuron. The secondary focus of this thesis is on the serotonin neuron and in particular the serotonin transporter (SERT), a marker of the serotonin neuron. To this end three distinct and separate models have been employed. The goals of this thesis were: (1) to test the hypothesis that monoamine oxidase inhibition during development alters serotonergic innervation in the cortex and raphe, while not affecting relative DA innervation of nigrostriatal pathway, (2) to test the hypothesis that elevated brain levels of hypoxanthine (Hx) deleteriously affect the DA neuron, and (3) to test the hypothesis that densities of DAT and SERT in brainstem cell body regions distinguish alcohol-preferring vervet monkeys with different behavioral patterns of ethanol consumption.
Alterations 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.
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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.

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Kim, 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.

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Hall, A. "Irreversibly binding dopamine analogues". Thesis, University of East Anglia, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355531.

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Caravona, Natalia Filomena. "Behaviour disorders dopamine-related". Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1042.

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Today there is a growing awareness that in Parkinson's disease can occur motor and non motor disorders, in particular substances dependency syndromes and behavioral addiction. Objectives of the study. Objective of the study is to determine any changes frontal circuits potentially involved in the development and maintenance of "behaviour addiction", by neuroimaging and neurophysiological methods in patients with Parkinson's disease with impulses control disorder. Materials and methods. In the study of 8 patients with Parkinson's disease with at least an impulse control disorder, particularly 8 pathological gambler , and 8 patients with non-demented Parkinson disease with comparable clinical and demographic characteristics who had not demonstrated behavioural abnormalities . Patients were subjected to a magnetic resonance imaging with conventional sequences and DWIs in 15 space directions (diffusion tensor imaging) and T1 weighted sequences volumetric, determination of P 300 neurophysiological and neuropsychological test battery for exploring the cognitive functions. Results. The two groups have had no statistically significant differences evaluated using t-Student test, although patients with ICDS have shown average levels of FA tend to higher; in assessing NP the only statistically significant differences have emerged the WCST and NPI. However, it should be pointed out as ICD patients, compared to Parkinsoniani without compulsive disorder, P3a monsters lower latency than the P3b, as evident in healthy subjects.
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Martin-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.

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A procedure was developed to determine the effect of a dopamine (DA) antagonist (haloperidol) and a DA agonist (d-amphetamine) on rats' perceptions of the hedonic value of food. Eighteen rats were trained to discriminate between two quantities of sweet food pellets (1 and 4), in a forced-choice two-lever successive discrimination procedure. To control for non-specific perceptual effects of the treatments, the rats were also trained to discriminate between 1 and 4 tones. It was established that rats attended to the value of food, as well as the proportional differences in quantity, when discriminating food quantities. This was accomplished by altering the value of the food in two ways. Firstly, "hunger" was altered by changing the degree of food deprivation during testing. Secondly, unsweetened food pellets were introduced as probe cues. These two methods of altering the value of food pellets were utilized while quantity generalization gradients were determined, by presenting animals with 1,2, 3 and 4 numbers of stimuli as probe cues. Two measures were derived from these generalization gradients: the point of subjective equality (PSE), which is the calculated number of stimuli that would maintain responses equally distributed between the two levers, and the slope of the gradient. The PSE primarily reflects perceptual processes, while the slopes of the gradients provide an index of performance impairment. It was observed that decreasing the value of food by either decreasing food deprivation or reducing the sweetness of the food pellets resulted in the rats perceiving a given quantity of food as larger than before these treatments (decreased the food PSE). Neither altering food deprivation nor introducing novel tone probes had an effect on the numerical attributes of tones, as reflected by the tone PSE. Haloperidol (0.030, 0.50 and 0.083 mg/kg, i.p.) produced a statistically significant, but slight dose-dependent performance deficit, as reflected by the slope of the generalization gradients. It did not affect the perception of food pellet quantities at any dose, as reflected by the food PSE. Haloperidol decreased the number of tones a given quantity was perceived as by rats (increased the tone PSE). Amphetamine (0.25, 0.50 and 1.0 mg/kg, i.p.) decreased the perception of a given quantity of food (increased the food PSE) in a dose-dependent manner, without a significant effect on performance. Thus, amphetamine enhanced the hedonic value of food. Amphetamine also increased rats' perceptions of a given number of tones (decreased the tone PSE). It therefore appears that while d-amphetamine can enhance the perceived hedonic value of food, haloperidol has no effect on rats' perceptions of the hedonic value of food. Furthermore, evidence that DA systems are involved in the mechanism of an "internal clock" or "counter" was obtained.
Medicine, Faculty of
Graduate
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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.

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IntroductionThe mesolimbic dopamine (DA) system is thought to be important for reward-based decision-making. Dysfunction of this system is implicated in impulsivity. Many neuropsychiatric disorders, such as drug addiction, obesity and pathological gambling, are characterized by a relative oversensitivity to reward and insensitivity to negative outcomes, as well as impulsivity. The administration of DA agonists in some patients with Parkinson's disease (PD) can trigger unusually risky behavior, such as pathological gambling and compulsive sexual behavior, which are impulse control disorders (ICD). Interestingly the risk factors predisposing PD patients to ICDs closely resemble those associated with drug addiction in the general population. PD patients who develop ICDs have risk factors similar to non-PD patients who develop addictions, possibly due to a similar underlying neurobiological mechanism. We asked two questions. 1) Are there underlying abnormalities in the neural processing of risky decision-making in PD, specifically those who develop ICDs? 2) What role does DA plays in risky decision-making in young healthy subjects: without the limiting factor of age, disease or pathology.MethodsExperiment 1 used functional magnetic resonance imaging (fMRI) to look at differences in neural activation during gambling in PD patients who had a history of ICDs due to DA agonist treatment (n=11, PD-ICD) compared to their disease (n=12, PD-CON) and age-matched controls (n=11, AM-CON). Experiment 2 tested the relationship between DA level and performance on a gambling and probabilistic selection task, using the acute phenylalanine/tyrosine depletion (APTD) method, fMRI and [11C]raclopride positron emission tomography (PET), in healthy subjects 18- 30 years of age (n=17). ResultsExperiment 1: (1) Individual predisposition to ICDs is evidenced by differences in personality, betting strategies and evaluation of financial risk. (2) The PD-ICD group showed dysfunction in the weighting of losses relative to gains both behaviourally and neurally. (3) The ventral striatal (VStr) reward prediction error signal is not necessary to develop and maintain behavioural addictions. And (4) Abnormality in the insular cortex's evaluation of risk and reward, and perhaps that of the mesocorticolimbic network in general, may be the main neural correlate mediating susceptibility for the development of an ICD in PD.Experiment 2: (1) APTD-induced lowering of brain DA led to an increase in loss aversion and an increased ability to learn from negative outcomes; the greater the depletion, the greater the improvement in punishment accuracy. (2) High impulsivity scores were correlated with high baseline D2 receptor levels, which may index low tonic DA and susceptibility to high phasic DA neuron firing. (3) The BOLD signal was correlated with the expected value and reward prediction error in the VStr bilaterally, however, this correlation was significantly increased after DA depletion, suggesting that the striatal BOLD signal in that area is not a direct result of DA release. Conclusion: The combination of both experiments resulted in four main conclusions: (1) the BOLD signal in the VStr may not be as DA driven as previously thought, (2) risk and loss aversion can be directly controlled by DA levels, (3) impulsivity, a risk factor for addiction and ICDs, is caused by an elevated phasic DA response to potential rewards, and (4) learning to avoid maladaptive choices is sensitive to acute changes in DA levels, possibly D2 receptor driven. The result of the present work provides a framework for understanding the reward and loss aversion systems that control risk taking, and impulsivity. Together, our results support a model in which impulsivity, a risk factor for addiction, is caused by an elevated phasic DA response to potential rewards, while learning to avoid maladaptive choices is sensitive to acute changes in DA levels, possibly D2 receptor driven.
IntroductionLe 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.
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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.

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Stevenson, 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.

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Stress activates dopamine (DA) transmission in the basolateral amygdala (BLA), medial prefrontal cortex (mPFC) and nucleus accumbens (NAc), and DA transmission in these regions mediates different aspects of the behavioural response to stress. Evidence indicates that a functional interdependence exists between the DA projections to these areas. mPFC DA exerts an inhibitory influence on stress-induced NAc DA release. Similarly, BLA DA modulates mPFC and NAc DA function, although it is unknown if this is also the case in response to stress. Thus, we examined whether BLA DA modulates NAc and mPFC DA release in response to stress. We first determined the effects of BLA DA depletion on stress-induced NAc and mPFC DA release. BLA DA depletion potentiated the NAc and attenuated the mPFC DA responses to stress. We then examined the effects of intra-BLA D1 and D2/D3 receptor antagonists on the NAc and mPFC DA responses to stress. BLA D1, but not D2/D3, receptor antagonism potentiated and attenuated stress-induced NAc and mPFC DA release, respectively. Co-administration of D1 antagonist into BLA and DA agonists into mPFC abolished the potentiation of stress-induced NAc DA release, indicating that BLA D1 receptor modulation of the NAc DA stress response occurs indirectly by modulating stress-induced mPFC DA release. We then turned to examining the influence of BLA DA on behavioural measures of information processing which are themselves modulated by NAc and mPFC DA function. The effects of BLA D1 and D2/D3 receptor blockade on prepulse inhibition (PPI) and latent inhibition (LI) were examined. BLA D1 receptor antagonist enhanced and D2/D3 receptor antagonist reduced PPI. Conversely, neither BLA DA receptor antagonist had an effect on LI. Finally, we determined the effects of BLA D1 and D2/D3 receptor antagonists on acoustic startle habituation. Although BLA DA receptor antagonism had no effect on this measure, both D1 and D2/D3 receptor blockade reduc
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Książki na temat "Dopamine"

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Kabbani, Nadine, red. Dopamine. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-251-3.

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Ian, Creese, i Fraser Claire M, red. Dopamine receptors. New York: A.R. Liss, 1987.

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L, Iversen Leslie, red. Dopamine handbook. New York: Oxford University Press, 2010.

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Tiberi, Mario. Dopamine receptor technologies. New York, NY: Humana Press, 2015.

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Tiberi, Mario, red. Dopamine Receptor Technologies. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2196-6.

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Monti, Jaime M., S. R. Pandi-Perumal i S. Chokroverty, red. Dopamine and Sleep. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46437-4.

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Neve, Kim A., red. The Dopamine Receptors. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-333-6.

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Neve, Kim A., i Rachael L. Neve, red. The Dopamine Receptors. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2635-0.

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A, Neve Kim, i Neve Rachael L, red. The dopamine receptors. Totowa, N.J: Humana Press, 1997.

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Akiyama, Watanabe, red. Dopamine research advances. New York: Nova Biomedical Books, 2008.

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Części książek na temat "Dopamine"

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Ahmed, Hesham M., Christopher T. Aquina, Vicente H. Gracias, J. Javier Provencio, Mariano Alberto Pennisi, Giuseppe Bello, Massimo Antonelli i in. "Dopamine". W Encyclopedia of Intensive Care Medicine, 760–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_278.

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Simola, Nicola, Micaela Morelli, Tooru Mizuno, Suzanne H. Mitchell, Harriet de Wit, H. Valerie Curran, Celia J. A. Morgan i in. "Dopamine". W Encyclopedia of Psychopharmacology, 417. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_588.

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Santos, Edalmarys, i Chad A. Noggle. "Dopamine". W Encyclopedia of Child Behavior and Development, 520. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_886.

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Treiber, Katherine, i Joann Tschanz. "Dopamine". W Encyclopedia of Clinical Neuropsychology, 883. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1762.

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Marinelli, Michela (Micky). "Dopamine". W Encyclopedia of Behavioral Medicine, 699–700. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_244.

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Upchurch Sweeney, C. Renn, J. Rick Turner, J. Rick Turner, Chad Barrett, Ana Victoria Soto, William Whang, Carolyn Korbel i in. "Dopamine". W Encyclopedia of Behavioral Medicine, 628–30. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_244.

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Vernon, Elizabeth, i Joann Tschanz. "Dopamine". W Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1762-3.

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Cosentino, Marco, i Franca Marino. "Dopamine". W Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5126-1.

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Vernon, Elizabeth K., i Joann Tschanz. "Dopamine". W Encyclopedia of Clinical Neuropsychology, 1209–10. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1762.

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Kruk, Zygmunt L., i Christopher J. Pycock. "Dopamine". W Neurotransmitters and Drugs, 87–115. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3132-2_4.

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Streszczenia konferencji na temat "Dopamine"

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Bedin, Andrea, Alexander Marinšek, Shaghayegh Shahcheraghi, Nairy Moghadas Gholian i Liesbet Van der Perre. "DOPAMINE". W CoNEXT '22: The 18th International Conference on emerging Networking EXperiments and Technologies. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3565474.3569072.

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Neel, Anna I., Alyssa M. West, Kimberly M. Holter, Monica H. Dawes, Katherine E. Liontis, Robert W. Gould, Sara R. Jones i Rong Chen. "Membrane Cholesterol Depletion Alters Striatal Dopamine Homeostasis and Dopamine-Associated Behavior". W ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.296.873200.

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Patil, Vidya, i Mugdha Patki. "Growth of dopamine crystals". W INTERNATIONAL CONFERENCE ON CONDENSED MATTER AND APPLIED PHYSICS (ICC 2015): Proceeding of International Conference on Condensed Matter and Applied Physics. Author(s), 2016. http://dx.doi.org/10.1063/1.4946478.

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Sharma, Sonika, i Banshi D. Gupta. "Fiber Optic SPR based Dopamine Sensor utilizing GNP/SnO2 Nanocomposite Sup-ported Molecular Imprinting". W JSAP-OSA Joint Symposia. Washington, D.C.: Optica Publishing Group, 2017. http://dx.doi.org/10.1364/jsap.2017.6a_a410_6.

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Dopamine (DA) belongs to the catecholamine family of neurotransmitters and is very important for humans. It is produced in adrenal glands and several areas of the brain. Dopamine is formed by decarboxylation of DOPA and is a precursor of two other neurotransmitters adrenaline and noradrenalin. Dopamine is the most abundant of the catecholamine, hence affects many aspects of brain functionality such as movement, emotional response and ability to experience pain and pleasure. Dopamine also affects the cardiovascular and renal systems. Excessive secretion of DA (e.g., due to Huntington’s disease) is associated with failure in energy metabolism and causes untimely death. Differently low levels of dopamine in the central nervous system causes several neurological diseases, for example schizophrenia, Parkinson’s disease. Therefore, it is important to detect dopamine level efficiently in human body [1].
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Ghosh, Dipannita, Md Ashiqur Rahman, Ali Ashraf i Nazmul Islam. "Graphene-Conductive Polymer-Based Electrochemical Sensor for Dopamine Detection". W ASME 2022 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/imece2022-96193.

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Abstract The central nervous system’s (CNS) dopaminergic system dysfunction has been linked to neurological illnesses like schizophrenia and Parkinson’s disease. As a result, sensitive and selective detection of dopamine is critical for the early diagnosis of illnesses associated with aberrant dopamine levels. In this research, we have investigated the performance of electrochemical screen-printed sensors for different concentrations of dopamine detection using graphene-based conductive PEDOT: PSS(G-PEDOT: PSS) and Polyaniline(G-PANI) inks on the working electrode and compared the sensitivity. SEM characterization technique has been performed to visualize the microstructures of the proposed inks. We have investigated cyclic voltammetry (CV) electrochemical techniques with ferri/ferrocyanide redox couple to assess the efficiency of the designed electrodes in detecting dopamine. G-PANI ink has shown to have better LOD and stability to detect dopamine with screen-printed electrodes. Further, we have also studied electrochemical analysis for the selective detection of dopamine without the interference of Ascorbic Acid (AA).
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Kulkarni, Tanmay, Deepa Gupta, Dan Covey, Joseph Cheer i Gymama Slaughter. "Dopamine sensing upon amphetamine administration". W 2015 IEEE Sensors. IEEE, 2015. http://dx.doi.org/10.1109/icsens.2015.7370580.

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Wang, Ran, Wei Yang, Yujing Luan, Jian Mao, Hong Qing i Yulin Deng. "Salsolinol, a Dopamine-derived Tetrahydroisoquinoline, Occur in Dopaminergic SH-SY5Y Cells Induced by Dopamine". W 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4381975.

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Bashford, Alison, Philip J. Clark i Rodrigo A. España. "Optogenetically modulating ventral tegmental area dopamine neuron activity alters dopamine transporter sensitivity to cocaine". W ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.312.100184.

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Enoch, Jay M., Gary L. Savage i Vasudevan Lakshminarayanan. "Psychophysical Tests of Dopamine Anomalies in the Retina". W Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/navs.1987.wd1.

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In recent years there has been great interest in the analysis of neurotransmitter substances and their role in vision and other central nervous system processes. Much evidence has accumulated implicating dopamine as a neurotransmiter in the retina. It is present in certain amacrine, interamacrine and interplexitorm cells (1-5, 8-10). As our knowledge about the role of dopamine in visual processing is limited, a key question to ask is, "are there functional visual effects due to anomalies of the dopamine system in the retina?".
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Yue, Kun, i Alice C. Parker. "Analog Neurons with Dopamine-Modulated STDP". W 2019 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2019. http://dx.doi.org/10.1109/biocas.2019.8919047.

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Raporty organizacyjne na temat "Dopamine"

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2009. http://dx.doi.org/10.21236/ada501075.

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2006. http://dx.doi.org/10.21236/ada452372.

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2005. http://dx.doi.org/10.21236/ada433063.

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Seegal, Richard F., Edward F. Fitzgerald, Eric S. Molho, Kenneth L. Marek i John P. Seibyl. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2003. http://dx.doi.org/10.21236/ada416007.

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2010. http://dx.doi.org/10.21236/ada517349.

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Carvey, Paul M. Cytokine Induction of Dopamine Neurons from Progenitor Cells. Fort Belvoir, VA: Defense Technical Information Center, październik 2000. http://dx.doi.org/10.21236/ada391417.

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2011. http://dx.doi.org/10.21236/ada593238.

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2007. http://dx.doi.org/10.21236/ada466563.

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Marek, Kenneth. Dopamine Transporter Imaging Assessment of Parkinson's Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2000. http://dx.doi.org/10.21236/ada383333.

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Seegal, Richard F. PCBs Alter Dopamine Mediated Function in Aging Workers. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2008. http://dx.doi.org/10.21236/ada478614.

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