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Academic literature on the topic 'Dopaminergic mechanisms'

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Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Dopaminergic mechanisms"

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Millichap, J. Gordon, and John J. Millichap. "Dopaminergic Mechanisms in Adhd." Pediatric Neurology Briefs 28, no. 1 (January 1, 2014): 8. http://dx.doi.org/10.15844/pedneurbriefs-28-1-10.

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Razzolini, R., P. Ostan, A. Ramondo, P. Stritoni, R. Chioin, and S. Dalla-Volta. "Dopaminergic mechanisms in heart failure." Pharmacological Research 22 (September 1990): 422. http://dx.doi.org/10.1016/s1043-6618(09)80432-5.

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Barone, P., K. S. Bankiewicz, G. U. Corsini, I. J. Kopin, and T. N. Chase. "Dopaminergic mechanisms in hemiparkinsonian monkeys." Neurology 37, no. 10 (October 1, 1987): 1592. http://dx.doi.org/10.1212/wnl.37.10.1592.

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IMAM, SYED Z. "Molecular Mechanisms of Dopaminergic Neurodegeneration." Annals of the New York Academy of Sciences 993, no. 1 (May 2003): 377. http://dx.doi.org/10.1111/j.1749-6632.2003.tb07547.x.

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Chen, Jianping. "Dopaminergic mechanisms and brain reward." Seminars in Neuroscience 5, no. 5 (October 1993): 315–20. http://dx.doi.org/10.1016/s1044-5765(05)80038-7.

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Lu, Jing-Shan, Qi-Yu Chen, Xiang Chen, Xu-Hui Li, Zhaoxiang Zhou, Qin Liu, Yuwan Lin, Miaomiao Zhou, Ping-Yi Xu, and Min Zhuo. "Cellular and synaptic mechanisms for Parkinson’s disease-related chronic pain." Molecular Pain 17 (January 2021): 174480692199902. http://dx.doi.org/10.1177/1744806921999025.

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Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease. Chronic pain is experienced by the vast majority of patients living with Parkinson’s disease. The degeneration of dopaminergic neuron acts as the essential mechanism of Parkinson’s disease in the midbrain dopaminergic pathway. The impairment of dopaminergic neurons leads to dysfunctions of the nociceptive system. Key cortical areas, such as the anterior cingulate cortex (ACC) and insular cortex (IC) that receive the dopaminergic projections are involved in pain transmission. Dopamine changes synaptic transmission via several pathway, for example the D2-adenly cyclase (AC)-cyclic AMP (cAMP)-protein kinase A (PKA) pathway and D1-G protein-coupled receptor kinase 2 (GRK2)-fragile X mental retardation protein (FMRP) pathway. The management of Parkinson’s disease-related pain implicates maintenance of stable level of dopaminergic drugs and analgesics, however a more selective drug targeting at key molecules in Parkinson’s disease-related pain remains to be investigated.
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Hughes, A., G. Martin, S. Thom, and P. Sever. "Dopaminergic Mechanisms in Human Peripheral Vasculature." Journal of Hypertension 3, no. 6 (December 1985): 664–65. http://dx.doi.org/10.1097/00004872-198512000-00024.

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Wood, Patrick B. "Mesolimbic dopaminergic mechanisms and pain control." Pain 120, no. 3 (February 2006): 230–34. http://dx.doi.org/10.1016/j.pain.2005.12.014.

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Riddle, Evan L., Annette E. Fleckenstein, and Glen R. Hanson. "Mechanisms of methamphetamine-induced dopaminergic neurotoxicity." AAPS Journal 8, no. 2 (June 2006): E413—E418. http://dx.doi.org/10.1007/bf02854914.

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Wickens, J. R., J. C. Horvitz, R. M. Costa, and S. Killcross. "Dopaminergic Mechanisms in Actions and Habits." Journal of Neuroscience 27, no. 31 (August 1, 2007): 8181–83. http://dx.doi.org/10.1523/jneurosci.1671-07.2007.

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Dissertations / Theses on the topic "Dopaminergic mechanisms"

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Bloomfield, Michael. "Dopaminergic mechanisms underlying psychosis." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/44332.

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Schizophrenia is a potentially devastating mental illness with a complex aetiology, in which the odds ratios for environmental risk factors for the disorder are greater than the odds ratios of any single gene hitherto identified. Within schizophrenia, striatal dopamine dysfunction has been proposed to underlie the development of psychosis. The Aberrant Salience hypothesis provides an explanatory model based on empirical findings to explain how psychotic symptoms may arise from striatal hyperdopaminergia, whereby multiple risk factors converge to elevate striatal dopamine synthesis capacity as the Final Common Pathway to psychosis. Two important epidemiological risk factors for the disorder are chronic cannabis use and longterm psychosocial stress, both of which have evidence supporting effects on the dopamine system. Environmental risk factors are by their very nature modifiable, and so this thesis examined whether these environmental risk factors were associated with the same dopaminergic abnormalities that have been observed in schizophrenia with 3,4-dihydroxy-6- [18F]-fluoro-l-phenylalanine Positron Emission Tomography. This thesis also examined whether cannabis users exhibit aberrant salience processing using a behavioural task, the Salience Attribution Task. This thesis found that long-term cannabis use was associated with reduced dopamine synthesis capacity and no relationship was found between striatal dopamine synthesis capacity and cannabis-induced psychotic-like symptoms. Whilst cannabis use was not associated with increased aberrant salience processing, there was a relationship between cannabis-induced psychotic-like symptoms and aberrant salience processing. This thesis found that long-term psychosocial stress is associated with reduced dopamine synthesis capacity, although this finding may be due confounding factors. However, a positive relationship was observed between childhood and recent adult stressors and dopamine synthesis capacity. These findings call into question the hypothesis that cannabis increases the risk of psychosis by inducing the same changes observed in schizophrenia, although there some evidence to support the hypothesis that psychosocial stressors do increase risk via this mechanism.
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Szostak, Carolyn Margaret. "Dopaminergic mechanisms in conditioned circling." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29438.

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After unilateral lesions of the mesotelencephalic dopamine (DA) system, the administration of DA receptor agonists results in circling. This response is believed to reflect an asymmetry in mesotelencephalic DA activity. Moreover, drug-induced circling is thought to be directed away from the projection of higher dopaminergic activity. Recently, it has been reported that circling can be established and maintained using operant procedures in surgically intact and drug naive rats. The phenomenon of conditioned circling has been associated with an asymmetrical change in DA metabolism within the striatum and nucleus accumbens. The present series of experiments was designed to characterize further the involvement of mesotelencephalic DA in conditioned circling. Rats trained to circle for water according to a continuous schedule of reinforcement did not exhibit increased DA metabolism within either the striatum or the nucleus accumbens (Experiment I). However, a bilateral augmentation was observed when rates of responding were increased by implementing an intermittent schedule of reinforcement (Experiment II). Concurrent increases in the biosynthesis of DA, as estimated by accumulation of DOPA following the administration of a DOPA decarboxylase inhibitor, were not observed (Experiment III). Experiments IVa and IVb examined the extent to which inherent directional biases, which play a role in determining the magnitude and direction of drug-induced circling, influenced the acquisition and performance of the conditioned circling response. No effects were evident. Moreover, a symmetrical, bilateral enhancement in DA metabolism was observed in the striatum, irrespective of directional preferences. While conditioned circling can be established and maintained by reinforcing the response with food, food itself influenced DA metabolism and therefore precluded the detection of changes in DA metabolism specific to the circling response. Specifically, striatal and accumbens DA metabolism was augmented to a similar extent in animals given matched amounts of non-contingently presented food (Experiment V). Concentrations of DA, DOPAC and homovanillic acid (HVA) were found to be differentially distributed throughout the striatum (Experiment Via), suggesting a possible chemical basis for the heterogeneity of striatal DAergic functions. Changes in striatal DA metabolism associated with conditioned circling were observed only within localized regions of the anterior striatum (Experiment VIb). All changes noted were, however, bilateral in nature. Finally, unilateral lesions of the mesotelencephalic DA projection, following the establishment of the conditioned circling response, disrupted responding, irrespective of the relative locus of the lesion (i.e. ipsilateral or contralateral to the direction of turning) (Experiment VII). However, the extent of the behavioral deficit was more severe following contralaterally placed lesions. It is concluded that circling, established and maintained by positive reinforcement, is subserved by a bilateral augmentation in DA metabolism within the nucleus accumbens and discrete regions of the striatum. However, lesion studies indicate an asymmetrical involvement of the ipsilateral and contralateral projections in this response.
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Stopper, Colin Michael. "Dopaminergic mechanisms guiding probabilistic choice." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46395.

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Racz, Karoly. "Peripheral dopaminergic mechanisms in experimental hypertension." Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72776.

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Pöltl, Dominik [Verfasser]. "Degeneration mechanisms in human dopaminergic neurons / Dominik Pöltl." Konstanz : Bibliothek der Universität Konstanz, 2012. http://d-nb.info/1025226135/34.

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Killcross, Andrew Simon. "Dopaminergic mechanisms and latent inhibition : implications for schizophrenia." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261541.

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Ferland, Jacqueline-Marie N. "Investigating the influence of risky decision making on dopaminergic reward mechanisms." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/63131.

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Addiction is a chronic relapsing psychiatric disorder affecting millions worldwide. Despite years of research investigating the etiology and phenomenology of substance abuse, there is no cure. Determining factors which promote the addictive phenotype may help to discover new therapeutics. Several clinical studies have shown addicts demonstrate poor cost/benefit decision making as measured by validated tasks such as the Iowa Gambling Task (IGT), a cognitive deficit maintained during periods of abstinence and associated with relapse risk. However, it is unclear whether disadvantageous choice precedes or is the consequence of drug abuse. Furthermore, dopaminergic signalling, actively recruited by drugs of abuse, has also been implicated in decision-making biases, and may contribute to choice deficits after drug exposure. The experiments here explored the role of disadvantageous choice in addiction susceptibility using rodent analogues of the IGT, the rat gambling task (rGT) and cued rat gambling task (crGT). These paradigms require the animal to choose between four different nose poke options which are associated with sugar wins, probabilities of winning, and timeouts. The crGT also includes salient reward-paired cues to enhance risky decision making. The first two experiments assessed whether baseline risk-preference on the rGT and crGT affected drug seeking as measured by cocaine self-administration, and whether drug exposure affected task performance. The third study examined the influence of task experience on the locomotor response to cocaine and responding for conditioned reinforcement, two dopamine-dependent behavioural assays associated with addiction risk. Basal and cocaine-induced nucleus accumbens dopamine release was also assessed using microdialysis after task training. The final study used chemogenetics to reduce nucleus accumbens dopamine to investigate the role of dopaminergic tone in choice biases. Our results show poor decision making precedes drug exposure, and is uniquely susceptible to drug-induced cognitive deficits. crGT rats showed greater drug seeking and sensitivity to cocaine-induced choice impairments, a phenotype linked to basal accumbal dopamine efflux. Finally, by reducing accumbens dopamine, animals showed marked reductions in risky choice. These data support the conclusion that poor decision making may serve as a cognitive endophenotype for addiction via aberrant dopaminergic signaling within the mesostriatal network.
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Narayanaswami, Vidya. "DIET-INDUCED OBESITY: DOPAMINERGIC AND BEHAVIORAL MECHANISMS AS OUTCOMES AND PREDICTORS." UKnowledge, 2013. http://uknowledge.uky.edu/pharmacy_etds/12.

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Obesity and drug abuse share common neural circuitries including the mesocoticolimbic and striatal dopamine reward system. In the current study, a rat model of diet-induced obesity (DIO) was used to determine striatal dopamine function, impulsivity and motivation as neurobehavioral outcomes and predictors of obesity. For the outcome study, rats were randomly assigned a high-fat (HF) or a low-fat (LF) diet for 8 wk. Following the 8-wk HF-diet exposure, rats were segregated into obesity-prone and obesity-resistant groups based on maximum and minimum body weight gain, respectively, and neurobehavioral outcomes were evaluated. For the predictor study, neurobehavioral antecedents were evaluated prior to an 8-wk high-fat diet exposure and were correlated with subsequent body weight gain. Striatal D2 receptor density was determined by in vitro kinetic analysis of [3H]raclopride binding. DAT function was determined using in vitro kinetic analysis of [3H]dopamine uptake, methamphetamine-evoked [3H]dopamine overflow and no net flux in vivo microdialysis. DAT cell-surface expression was determined using biotinylation and Western blotting. Impulsivity and food-motivated behavior were determined using a delay discounting task and progressive ratio schedule for food-reinforcers, respectively. Relative to obesity-resistant, obesity-prone rats exhibited 18% greater body weight, 42% lower striatal D2 receptor density, 30% lower total DAT expression, 40% lower in vitro and in vivo DAT function, 45% greater extracellular dopamine concentration, and 2-fold greater methamphetamine-evoked [3H]dopamine overflow. Obesity-prone rats exhibited higher motivation for food, but were less impulsive relative to obesity-resistant rats. Neurobehavioral antecedents of DIO included greater motivation for high-fat reinforcers in rats subsequently shown to be obesity-prone relative to obesity-resistant. Impulsivity, DAT function and extracellular dopamine concentration did not predict the DIO-phenotype. Thus, motivation for food is linked to both initiation and maintenance of obesity. Importantly, obesity results in decreased striatal DAT function, which may underlie the maintenance of compulsive food intake in obesity.
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Bradley, Curtis. "Examining the Associative Learning and Accumbal Dopaminergic Mechanisms of Caffeine Reinforcement." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3457.

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Caffeine is the most consumed psychoactive substance in the world, and most caffeine consumption in coffee and energy drinks is intended to produce a psychoactive effect. However, caffeine is not a primary reinforcer in preclinical paradigms – non-human species do not reliably take the drug to produce a psychoactive effect. However, caffeine is a ‘reinforcement enhancer’ in preclinical models; the effects of caffeine increase the motivation to obtain other non-drug reinforcers. The overall goal of this project was to determine if these reinforcement enhancing effects of caffeine could promote caffeine self-administration and to subsequently investigate the behavioral and neurochemical underpinnings of this effect. We hypothesized reliable caffeine self-administration would occur by adventitious pairing of caffeine with saccharin, a primary reinforcer. Second, we hypothesized that caffeine enhances reinforcement by increasing the salience of incentive stimuli, which are stimuli that come to evoke approach behaviors through associative learning (e.g., Pavlovian conditioning). Finally, incentive salience is moderated by dopamine release in the nucleus accumbens (NAc), an area highly involved in reward-learning and substance dependence. Therefore, we hypothesized that if caffeine enhanced control of approach behavior by incentives, then it would increase the ability of incentive stimuli to evoke dopamine in the NAc. These studies show that intravenous delivery of caffeine with oral saccharin increases operant relative to control groups responding for intravenous caffeine or oral saccharin. The effect was also dose-dependent, confirming that the psychoactive effects of caffeine increased behavior. We also extended this effect to an oral model of caffeine self-administration, which included a simple sweetener (saccharin) or a complex oral vehicle (saccharin with decaffeinated coffee) to mask the bitter taste of caffeine. Presenting caffeine with oral saccharin promoted self-administration, relative to saccharin alone and did not depend on the nature of the complexity of the vehicle. Caffeine also dose-dependently increased approach to an incentive stimulus and this effect was associated with increased extracellular dopamine in the NAc. These findings suggest caffeine enhances incentive motivation and that this effect may result from increases in CS-evoked striatal dopamine.
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Daniel, James St Vincent Clinical School UNSW. "Studies of neurotransmitter release mechanisms in dopamine neurons." Awarded by:University of New South Wales. St. Vincent Clinical School, 2007. http://handle.unsw.edu.au/1959.4/31934.

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Medications that treat diseases such as Parkinson???s disease work by regulating dopamine transmission at synapses. Surprisingly, little is known about the mechanisms regulating dopamine release at synapses. In this thesis, we study mechanisms that regulate vesicle recycling in axons and dendrites of dopamine neurons. Key questions we addressed were: (1) Are vesicles in axons and dendrites associated with the same regulatory proteins, and thus by implication the same regulatory mechanisms, as in excitatory neurons; (2) Do vesicles undergo recycling, and (3) if so, are they characterised by a distinct pool size and rate of recycling. To study this, we cultured dopamine neurons and used immunocytochemistry to detect vesicular monoamine transporter 2 (VMAT2) and identify axons, dendrites and synaptic proteins, combined with labelling of recycling vesicles using FM 1-43. Vesicles in axons, but not in dendrites, were associated with presynaptic proteins such as Synaptophysin and Bassoon. We identified two kinds of presynaptic sites in axons: ???synaptic??? (located close to soma and dendrites??? and ???orphan???. The recycling vesicle pool size was smaller at orphan sites than at synaptic sites, and the initial rate of vesicle pool release was also lower at orphan sites. Both synaptic and orphan sites exhibited lower rates of vesicle pool release compared to hippocampal synapses, suggesting functional differences in presynaptic physiology between dopamine neurons and hippocampal neurons. In somatodendritic regions, VMAT2 was localised to the endoplasmic reticulum, Golgi, endosome, and large dense-core vesicles, suggesting that these vesicles might function as a part of the regulated secretory pathway in mediating dopamine release. None of the synaptic vesicle proteins we studied were detected in these regions, although some preliminary evidence of vesicle turnover was detected using FM 1-43 labelling. This thesis provides a detailed analysis of neurotransmitter release mechanisms in dopamine neurons. Our data suggests that presynaptic release of dopamine is mediated by mechanisms similar to those observed in excitatory neurons. In somatodendritic regions, our data suggests that VMAT2 is localised to organelles in secretory pathways, and that distinct mechanisms of release might be present at somatodendritic sites to those present in presynaptic sites. This thesis provides novel methods for analysing vesicle recycling in dopamine neurons, which provides the basis for further studies examining presynaptic function of dopamine neurons in normal brain function, disease, and therapeutic approaches.
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Books on the topic "Dopaminergic mechanisms"

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1937-, Bodis-Wollner Ivan, Piccolino Marco, and International Brain Research Organization. Congress, eds. Dopaminergic mechanisms in vision. New York: Liss, 1988.

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R, Ashby Charles, ed. The modulation of dopaminergic neurotransmission by other neurotransmitters. Boca Raton: CRC Press, 1996.

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Kujacic, Mirjana. Dopaminergic control of adrenomedullary function in the rat. Göteberg [Sweden]: Dept. of Pharmacology, University of Göteberg, 1994.

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P, Riederer, ed. The Role of brain dopamine. Berlin: Springer-Verlag, 1989.

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Paul, Willner, Scheel-Krüger Jørgen, and European Behavioral Pharmacology Society, eds. The mesolimbic dopamine system: From motivation to action. Chichester: Wiley, 1991.

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Miller, Robert, 1943 Aug. 29- and Wickens J, eds. Brain dynamics and the striatal complex. Amsterdam, Netherlands: Harwood Academic, 2000.

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Anton, Reiner, ed. Phylogeny and development of catecholamine systems in the CNS of vertebrates. Cambridge: University of Cambridge Press, 1994.

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Kjell, Fuxe, and Wenner-Grenska samfundet, eds. Trophic regulation of the basal ganglia: Focus on dopamine neurons. Oxford, OX, UK: Pergamon, 1994.

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W, Stone T., ed. CNS neurotransmitters and neuromodulators: Glutamate. Boca Raton: CRC Press, 1995.

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C, Baron J., and European Economic Community, eds. Brain dopaminergic systems: Imaging with positron tomography : proceedings of a workshop held in Caen, France, within the framework of the European Community medical and public health research. Dordrecht: Kluwer Academic Publishers, 1991.

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Book chapters on the topic "Dopaminergic mechanisms"

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Memo, M., C. Missale, L. Castelletti, M. Pizzi, and P. F. Spano. "Transduction Mechanisms at Dopamine Receptors." In Dopaminergic Systems and their Regulation, 153–63. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_10.

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Farsang, Csaba, and Alexander Alföldi. "Opioidergic-Dopaminergic Interaction in Hypertension." In Central Neural Mechanisms in Cardiovascular Regulation, 265–75. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4615-9834-3_19.

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Felder, Robin A., Robert M. Carey, and Pedro A. Jose. "The Renal Dopaminergic System, Hypertension, and Salt Sensitivity." In Hypertension and Hormone Mechanisms, 159–72. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_10.

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Albert, Paul R., Mohammad H. Ghahremani, and Stephen J. Morris. "Mechanisms of Dopaminergic Regulation of Prolactin Secretion." In The Dopamine Receptors, 359–81. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2635-0_12.

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Stone, Richard A., Ton Lin, P. Michael Luvone, and Alan M. Laties. "Postnatal Control of Ocular Growth: Dopaminergic Mechanisms." In Ciba Foundation Symposium 155 - Myopia and the Control of Eye Growth, 45–62. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514023.ch4.

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Raiteri, M., G. Bonanno, A. Caviglia, M. Rottigni, and M. Marchi. "Mechanisms Underlying the Modulation of Dopamine Release through Presynaptic Muscarinic Receptors." In Dopaminergic Systems and their Regulation, 35–43. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_3.

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Huffman, Ronald D., Maharaj K. Ticku, and Joseph M. Frey. "Gabaergic Mechanisms after Manipulation of Striatal Dopaminergic Neurons." In Pharmacology and Functional Regulation of Dopaminergic Neurons, 219–25. London: Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-10047-7_35.

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Clopton, J. K., and J. H. Gordon. "Separate Molecular Mechanisms for Estrogen-induced Up- and Down-regulation of Striatal Dopamine Receptors." In Dopaminergic Systems and their Regulation, 293–302. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_20.

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Glowinski, J., Y. Torrens, and J. C. Beaujouan. "The Striatonigral Substance P Pathway and Dopaminergic Mechanisms." In Novartis Foundation Symposia, 281–95. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720738.ch16.

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Diana, M., Z. L. Rossetti, and G. L. Gessa. "Central Dopaminergic Mechanisms of Alcohol and Opiate Withdrawal Syndromes." In Drug Addiction and Related Clinical Problems, 19–26. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-6901-8_3.

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Conference papers on the topic "Dopaminergic mechanisms"

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Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.

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Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.
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Wong, S. T., J. G. Sivak, A. K. Bal, M. G. Callender, and A. J. Bakelaar. "Changes in Amacrine Cell Numbers and Morphology in Response To Induced Myopia and Hyperopia." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1998. http://dx.doi.org/10.1364/vsia.1998.suc.2.

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Myopia and hyperopia have been artificially induced in animal models by various manipulations of their early visual environment. Ametropias have been produced using lid suture1, changing illumination levels (dark-rearing2, constant light3, dim lighting4), intra-ocular injections5, treatment with defocussing lenses6, and the application of translucent occluders7. Abnormal ocular growth appears to be a major factor that causes ametropia. Myopic eyes are enlarged, while hyperopic eyes are smaller compared to control eyes. Changes in the sclera8, choroid9, and orbital bone10 surrounding the affected eyes also reflect abnormal growth mechanisms. Various studies11,12,13 suggest that the signal or signals which control eye growth may arise from within the retina itself. It has been suggested that retinal amacrine cells play a role in mediating ocular growth8. This study examines how dopaminergic and serotonergic amacrine cells are quantitatively and qualitatively affected by induced myopia and hyperopia.
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Pinheiro, Amanda Pereira Sindeaux, Pedro Vitor Ferreira Rodrigues, Raoni de Oliveira da Silva Domingues, and Leonardo José Rodrigues Araújo Melo. "Gastrointestinal dysmotility associated with Parkinson’s disease’s mechanism." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.461.

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Introduction: Parkinson’s Disease (PD) is a condition of the brain that consiste of the death of dopaminergic neurons in the substantia nigra, therefore causing dyskinesias and dystonias. Besides the motor symptoms, the neurogastro motility is affected by the disease, since gastrointestinal dysfunction is a frequent and clinically relevant symptom of PD. Objectives: To link the neural pathways and neurotransmitters that involve the neuroenteric system control and the PD’s pathology. Methods: A systematic literature review was performed based on data extraction through the advanced research engine from Pubmed. Publications with the descriptors “dysmotility” OR “gastro motility” AND “Parkinson” were selected. Results: Through clinical and pre-clinical studies on PD, there has been hypothesized a gut-brain axis that is connected through hormones, neurotransmitters and dopamanergic inputs. This hypothesis is supported by evidence in the showing of accumulation of alpha-synuclein in the vagal system and Enteric Nervous System, the use of drugs such as peripheral dopaminergic blockers and serotonin for gastroparesis, the ghrelin effects on the central dopaminergic system through modulation of the mesencephalic dopaminergic signaling tested on rats, the gastrointestinal autonomic neuropathy detected in PD patients and the establishment of gut dysmotility before motor onset symptoms. Therefore, dysmotility isues such as delayed gastric emptying may not only be a symptom of PD, but also contrubute to the pathogenesis itself through impaired signaling. Conclusion: The gut-brain axis can be not only a tool for PD diagnosis but also a treatment target to restrain the advance of the disease. Although many articles are related this subject, there is a lack of designed trials for atypical movement disorders. To explore the dysmotility in PD, there is a need for multi-modality standardized tests to evaluate severity and prevalence.
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Chaprov, Kirill, Valeria Goloborshcheva, Ekaterina Teterina, Valeriayn Kucheryanu, Sergey Morozov, and Ruslan Ovchinnikov. "STUDIES OF THE ROLE OF SYNUCLEIN FAMILY PROTEINS IN THE MECHANISM OF TOXIN-INDUCED DAMAGE OF SUBSTANTIA NIGRA DOPAMINERGIC NEURONS." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1325.sudak.ns2020-16/505-506.

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