Dissertations / Theses on the topic 'Dopaminergici'
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GAMBARDELLA, Cristina. "Caratterizzazione della corrente h in neuroni dopaminergici della substantia nigra pars compacta." Doctoral thesis, Università degli studi di Ferrara, 2011. http://hdl.handle.net/11392/2388763.
Full textGIUSTIZIERI, MICHELA. "Meccanismi di modulazione presinaptica nei neuroni dopaminergici della substantia nigra pars compacta." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/561.
Full textPresynaptic inhibition is a mechanism of synaptic modulation normally observed in the synapses of the nervous system. This process starts upon activation of a large number of presynaptic receptors and leads to the decreased probability of vesicles to fuse to the cell membrane. One of the most common mechanism consists in the inhibition of the voltage dependent calcium channels (VDCC) located on the active zone of the presynaptic neuron. However, there is evidence for another form of presynaptic inhibition with a direct impairment of the vescicular release machinery. In my thesis I have investigated the mechanisms of presynaptic inhibition by group III metabotropic glutamate receptors (mGluRs) and GABAB receptors of the GABAergic neurotransmission to dopamine (DA) neurones of the rat substantia nigra pars compacta (SNc). The group III mGluRs agonist L-(+)-2-amino-4-phosphonobutyric acid (AP4, 100 μM) and the GABAB receptor agonist baclofen (10 μM) reversibly depressed the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) to 48.5 ± 3.7 % and 83.6 ± 2.3 % of control, respectively, with no effect in their amplitude. AP4 did not affect miniature inhibitory postsynaptic currents (mIPSCs) recorded in tetrodotoxin (TTX, 1 μM) and cadmium (100 μM), while in TTX (1 μM) and barium (1 mM), mIPSCs frequency was reduced to 75.3 ± 2.8 % of control. In contrast, baclofen reduced mIPSCs frequency either in cadmium (70.0 ± 6.7 % of control) or barium (52.3 ± 2.9 % of control). In TTX and ionomycin (2 μM), baclofen significantly reduced mIPSCs frequency to 71.8 ± 6.9 % of control, while AP4 had no effect. Similarly, in TTX and α-latrotoxin (α-LTX, 0.3 nM), the frequency of mIPSCs was reduced by baclofen to 64.5 ± 4.8 % of control, but was insensitive to AP4. Finally, in the continuous presence of baclofen, AP4 failed to produce any further reduction of sIPSCs frequency. The conclusion of this study is that group III mGluRs depress GABA release to DA neurons of the SNc through inhibition of presynaptic voltage-dependent calcium channels, while presynaptic GABAB receptors also impair transmitter exocytosis, and both mechanisms coexist on the same synapses. This characterization provides new insights about the role of these presynaptic receptors in the physiology of the substantia nigra and their potential involvement in the treatment of neurodegenerative diseases such as Parkinson’s Disease.
LALLAI, VALERIA. "L’isolamento sociale riduce marcatamente la risposta dei neuroni dopaminergici mesocorticali agli stimoli piacevoli." Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266621.
Full textCUCCHIARONI, MARIA LETIZIA. "Meccanismi di vulnerabilità dei neuroni dopaminergici mesencefalici di ratto esposti a fattori neurotossici ambientali." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/848.
Full textIt is well known that several neurodegenerative diseases, such as Parkinson disease, have a multifactorial origin (multiple hit hypothesis), which suggests that neuronal loss is a result of multiple factors. Among them, environmental factors are the most important. Although a variety of neurological processes can be adversely affected, the dopaminergic system appears to be a major target for environmental neurotoxins. The hypothesis that L-BMAA (L-β-methylamino-L-alanine), a nonprotein amino acid found in the Cycas micronesica seeds in western pacific islands, is involved in the development of amyotrophic lateral sclerosis/Parkinson-dementia complex (ALS-PDC complex) has risen and fallen since its initial proposal in 1987. In the last ten years the interest for this toxin has grown due to the discovery that it can be produced by many strains of Nostoc cyanobacterias, present throughout the world. Moreover L-BMAA can bind proteins. This bound form may function as an endogenous neurotoxic reservoir, accumulating and being released during protein catabolism. In order to analyze the effects of this amino acid, we have performed electrophysiological, pharmacological, morphological and toxicological studies on dopaminergic neurons of SNc. In these neurons puff-application of L-BMAA (3 mM, 10 psi 1.0 s) causes an inward current (mean = 454.48 34.65, n = 73) and a transient increase of intracellular calcium (R mean = 0.368 ± 0.062, n = 13). These effects are mediated by the activation of group I metabotropic glutamate receptors (mGluR1) and they are reversibly blocked by the application of the antagonist CPCCOEt (100 μM) (current: 41.56 ± 3.61 % of control, n = 24; calcium: 28.43 ± 5.96 % of control, n = 7). Bath application of CNQX (10 μM), a competitive antagonist of AMPA receptors, partially inhibits the L-BMAA-induced current (current: 93,09 ± 1,97 % of control, n = 24) but it has no effect on the calcium concentration (100.17 ± 9.93 % of control, n = 6). SOCs/TRPC channels are present in the dopaminergic cells of SNc and they mediate the intracellular calcium increase due to the activation of mGluR1. Indeed SKF 96365 (100 μM) and Ruthenium Red (20 μM), two antagonists of TRPC channels, are able to reduce the L-BMAA-induced inward current (42.125 ± 4.35 % of control, n = 8 and 27.05 ± 8.3 % of control, n = 6 respectively). Moreover SKF 96365 (100 μM) reduces the intracellular calcium increase induced by L-BMAA (43.57 ± 7.9 % of control). It is known that L-BMAA, in the presence of carbonate, has a chemical structure similar to glutamic acid, however it is not re-uptaken by EAATs, the excitatory amino acid transporters. Interestingly, in GABAergic interneurons, L-BMAA activates AMPA receptors but not mGluR1, and this activation causes inward current without any change in intracellular calcium concentration. However mGluR1 are present in these neurons because application of DHPG (30 μM), the selective agonist, produces inward currents. In order to confirm the toxic effects of this amino acid we have treated midbrain slices with L-BMAA for 12, 20 and 30 minutes and we have seen irreversible modification of cellular properties (decrease in membrane resistance, inability to evoke firing, elevated intracellular calcium). As a consequence of the treatments, cytocrome C is released in the cytoplasm, but in the presence of AMPA and mGluR1 antagonists, this effect is blocked. In conclusion this study demonstrates that L-BMAA could be considered a possible toxic agent for the dopaminergic neurons and provides new insights into the role of this amino acid in the aetiology of Parkinson disease.
ANGIONI, LAURA. "Ossitocina nella Sostanza Nera del ratto: azione sull'attività locomotoria e interazione con i neuroni dopaminergici, glutammatergici e GABAergici nigrali." Doctoral thesis, Università degli Studi di Cagliari, 2016. http://hdl.handle.net/11584/266640.
Full textESPA, ELENA. "Meccanismo d'azione del Pramipexolo nella terapia della malattia di Parkinson." Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266366.
Full textCAVALLERI, LAURA. "Generazione e caratterizzazione di neuroni dopaminergici mesencefalici umani derivati da cellule staminali pluripotenti indotte da utilizzarsi come componente di dispositivi terapeutici per parkinsonismi." Doctoral thesis, Università degli studi di Modena e Reggio Emilia, 2022. http://hdl.handle.net/11380/1273446.
Full textThe degeneration of dopaminergic (DA) neurons of the ventral mesencephalon is considered one of the hallmarks in Parkinson’s disease (PD) and Parkinsonism. Their susceptibility to damage and their adaptability and plasticity were initially studied in animal models in order to understand the cellular and molecular mechanisms and the action of pharmacological therapeutics. The recent introduction of human inducible pluripotent stem cells (iPSCs) technology and the development of protocols for their differentiation into neurons with a DA phenotype has permitted the direct evaluation of cellular mechanisms of PD and Parkinsonism, the mechanism of action of anti-parkinsonian drugs and the exploratory applications of various aspects of cell therapy. The aim of this thesis was the generation and phenotypic characterization of human DA neurons amenable to be used as a tool for the development of a variety of therapeutic devices based on cell therapy, in particular implantable whole-organic electronic devices. These devices were designed to be implanted in animal models of PD for a loco-regional therapy driven by electrical and chemical stimuli to support the engraftment of DA neuron precursors, maximizing their differentiation and function. In order to achieve high quality and reproducible human DA neuron precursors that are able to differentiate and mature into functional DA neurons that respond to electrical and chemical stimuli, therefore amenable to the above described use, this work was organized in four main subprojects. The first subproject was dedicated to the optimization of the methods of differentiation of human iPSCs into mesencephalic DA neuron precursors using a previously published protocol (Fedele et al. 2017). These DA neuron precursors can be expanded for several passages and stored in liquid nitrogen for any future use. The second subproject was dedicated to the differentiation of mesencephalic DA precursors into mature DA neurons that were characterized by immunofluorescence, quantitative PCR, HPLC and electrophysiological analyses. The DA phenotype of the neurons was investigated by testing their response to two dopaminergic agonists (i.e., pramipexole and piribedil) currently used for the treatment of PD. Recent data have demonstrated a neurotrophic effect produced by an anti-parkinsonian DA D2/D3 receptor (D2R/D3R) agonist, ropinirole (Collo et al. 2018). Based on these findings, the cellular and molecular effects of pramipexole and piribedil on human DA neurons were evaluated by studying morphological changes related to structural plasticity and the activation of intracellular pathways. The neuroprotective and neuroregenerative properties of these two pharmacological agents were also studied. The third subproject was dedicated to the study of the effects of the electrical stimulation on the structural plasticity of human DA neurons. Several reports have shown that electrical stimulation can promote neuronal differentiation and neurite growth of various neuronal cell types in vitro, including PC12 (Jing et al. 2019) and human neural stem cells (Stewart et al. 2015). The fourth subproject was dedicated to the generation of human iPSCs from peripheral blood mononuclear cells (PBMCs) donated from a novel set of healthy controls and patients affected by a Parkinsonism, i.e., the multiple system atrophy (MSA). The iPSC clones obtained from the control and the patient underwent a phenotypic characterization to examine the presence of pluripotency markers by immunofluorescence and quantitative PCR analysis, karyotype analysis, pluripotency and trilineage differentiation potential. The iPSCs were subsequently differentiated into mesencephalic DA neurons and assessed for their pharmacological response to dopaminergic agonists.
SCIAMANNA, GIUSEPPE. "La disfunzione del recettore striatale D2 induce un’alterata trasmissione GABAergica in un modello murino di distonia DYT1." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/849.
Full textDYT1 dystonia is a severe form of inherited generalized dystonia, caused by a deletion in the DYT1 gene encoding the protein torsinA. The physiological function of torsinA is unclear, though it has been proposed to perform chaperone-like functions, assist in protein trafficking, membrane fusion and participate in secretory processing. Alterations in GABAergic signaling have been involved in the pathogenesis of dystonia. I recorded GABA- and glutamate-mediated synaptic currents from striatal neurons obtained from a mouse model of DYT1 dystonia. In medium spiny neurons (MSNs) from mice expressing human mutant torsinA (hMT), we observed a significantly higher frequency, but not amplitude, of GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) and miniature currents (mIPSCs), whereas glutamatergic spontaneous excitatory synaptic potentials (sEPSCs) activity was normal. No alterations were found in mice overexpressing normal human torsinA (hWT). To identify the possible sources of the increased GABAergic tone, I recorded GABAergic Fast-Spiking (FS) interneurons that exert a feed-forward inhibition on MSNs. Both sEPSC and sIPSC recorded from hMT FS interneurons were comparable to hWT and controls.In physiological conditions, dopamine (DA) D2 receptor act presynaptically to reduce striatal GABA release. Notably, application of the D2-like receptor agonist quinpirole failed to reduce the frequency of sIPSCs in MSNs from hMT as compared to hWT and controls. Likewise, the inhibitory effect of quinpirole was lost on evoked IPSCs both in MSNs and FS interneurons from hMT mice. My findings demonstrate a disinhibition of GABAergic synaptic activity, that can be partially attributed to a D2 DA receptor dysregulation. A rise in GABA transmission would result in a profound alteration of striatal output, that might be relevant to the pathogenesis of dystonia.
Bloomfield, Michael. "Dopaminergic mechanisms underlying psychosis." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/44332.
Full textSzostak, Carolyn Margaret. "Dopaminergic mechanisms in conditioned circling." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29438.
Full textMedicine, Faculty of
Graduate
Stopper, Colin Michael. "Dopaminergic mechanisms guiding probabilistic choice." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46395.
Full textMaci, Tiziana. "Dopaminergic System and cognitive function." Thesis, Universita' degli Studi di Catania, 2011. http://hdl.handle.net/10761/100.
Full textPatients with Parkinson's disease (PD) have been reported to have deficient temporal processing. The effects of L-dopa therapy on time evaluation are not yet clear; in fact both positive and negative effects have been observed. The present investigation was designed to analyze the capability of estimating short as well as long time intervals in PD patients and the effect of dopamina replacement by L-dopa administration. Ten PD patients were compared with 10 age- and education-matched controls. We evaluated the capability of estimating time intervals in the range from 1 to 5 s (short intervals) as well as from 40 to 90 s (long intervals). For the time estimation, we used tasks requiring internal count as well as tasks that did not allow it. In PD patients, the effects of L-dopa on time estimation was assessed by comparing the results obtained before (OFF) and two hours after drug administration (ON). Time estimation of short intervals, when the internal count was allowed, demonstrated that patients with PD in OFF state perceived the time intervals longer than usual compared to normal controls. This condition normalized in ON state, being not significantly different from normal subjects. When internal counting was not allowed, PD patients in OFF state performed worse than normal subject, but L-dopa administration, instead to normalize the condition, increased the error rate in ON state. In the estimation of long time intervals, PD patients in OFF state displayed only a modest impairment, slightly improved by L-dopa intake, in both conditions (counting or not counting). In patients with PD, the time estimation is dependent from dopamine availability. For short time intervals estimation, L-dopa had a paradoxical dual action, ameliorating the estimates when motor mechanisms (internal counting) were presumably involved and worsening the estimates when other cognitive mechanisms were requested (qualitative evaluation). Moreover, the different behaviors following L-dopa administration observed for short and long estimates suggest the involvement of different internal timers.
DE, SANCTIS Claudia. "MicroRNAs profiling in Dopaminergic neurons." Doctoral thesis, Università degli studi del Molise, 2018. http://hdl.handle.net/11695/83499.
Full textMidbrain dopaminergic neurons (mDA) development is a complex and still not fully understood phenomenon. Many studies till now concentrated their attention on the roles played by several, specific and well-known transcription factors. The aim of my PhD thesis is focus on a relatively new class of post-transcriptional regulators named microRNAs (miRNAs) able to regulate gene expression by targeting partially complementary sequences in the 3’untranslated regions (UTRs) of the target mRNAs. To investigate the role played by miRNAs during mDA differentiation, we choose to analyze miRNAs expression profile by using miRNA Array platforms. To this purpose we used an optimized protocol from mouse Epiblast stem cells (epiSC) differentiated into DA neurons (Jeager et al. 2011). By bioinformatics analysis of the array data, obtained from epiSC differentiated into mDA neurons, we identified few candidates most likely implicated in the DA neurons differentiation and function. The candidate miRNAs were screened for their ability to induce DA phenotype. To this purpose, I generated inducible lentiviral vectors for each miRNA and I have infected mesencephalic primary cultures from mice at stage E12.5. Among all candidate miRNAs, miR-218 and miR-34b/c increase the number of TH+ positive cells, showing their possible contribution in the mDA neurons. Moreover, miR-218 and miR-34b/c, were enriched both in midbrain of mice (E13.5) and in FACS sorted GFP+ cells isolated from E13.5 Pitx3-GFP mice embryos when compared with control. Data obtained from Luciferase Assay and Dual Fluorescence Reporter Assay suggest that miR-34b/c target and suppress Wnt1 3’UTR and it is expressed during DA neurons differentiation. By performing In situ hybridization analysis and immunohistochemistry, I was able to detect miR-218 in particular in the mouse midbrain at stage E14, where co-localize rostrally with Isl-1 (motor neuron marker) and caudally with TH, Pitx3, Lmx1a (dopaminergic marker). This data suggests that miR-218 is expressed also in cranial motor neurons, as described in others recent studies (Thiebes, K.P. et al. 2014; Amin, N.D et al. 2015). To further understand the role of miR-218 in development and function of dopaminergic neurons I have generated the conditional knock-out (cKO) mice for miR-218-2. By mating miR-218-2 flox/flox with En1Cre/+ mice expressing the Cre under Engrailed 1 promoter (En1 is a pro-dopaminergic marker) I will be able to investigate the contribution of miR-218 in dopaminergic system. Preliminary observations on miR-218-2 flox/flox En1Cre/+ mice shown motor impairment phenotype, but to confirm this data I’m currently performing behavior tests and in vivo analysis. Through miRNA expression profiling we be able understand mechanism and function of dopaminergic system, because miRNAs are as key regulators in gene expression networks, can influence many biological processes and have also shown promise as biomarkers for neuro-disorders.
Zietlow, Rike. "Factors affecting the survival of embryonic dopaminergic neurones after transplantation." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624313.
Full textLak, Armin. "Encoding of economic value by midbrain dopamine neurons." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648342.
Full textPES, ROMINA. "Ruolo dei neurosteroidi nella modulazione dopaminergica." Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266803.
Full textAron, Liviu. "Genetic analysis of dopaminergic neuron survival." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-117874.
Full textRacz, 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.
Full textLokwan, S. J. A. "Excitatory regulation of central dopaminergic neurones." Thesis, Swansea University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.637946.
Full textFallon, S. J. "Dopaminergic modulation of planning and attention." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598929.
Full textDommett, Eleanor Jane. "Sensory regulation of midbrain dopaminergic neurons." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425614.
Full textVander, Weele Caitlin Miya. "Dopaminergic modulation of prefrontal cortex subpopulations." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/120628.
Full textCataloged from PDF version of thesis. Page 176 blank.
Includes bibliographical references (pages 159-175).
Despite abundant evidence that dopamine modulates medial prefrontal cortex (mPFC) activity to mediate diverse behavioral functions, the precise circuit computations remain elusive. One potentially unifying theoretical model by which dopamine can modulate functions from working memory to schizophrenia is that dopamine serves to increase the signal-to-noise ratio in mPFC neurons, where neuronal activity conveying sensory information (signal) are amplified relative to spontaneous firing (noise). To connect theory to biology, we lack direct evidence for dopaminergic modulation of signal-to-noise in neuronal firing patterns in vivo and a mechanistic explanation of how such computations would be transmitted downstream to instruct specific behavioral functions. Here, we demonstrate that dopamine increases signal-to-noise ratio in mPFC neurons projecting to the dorsal periaqueductal gray (dPAG) during the processing of an aversive stimulus. First, using electrochemical approaches, we reveal the precise time course of tail pinch-evoked dopamine release in the mPFC. Second, we show that dopamine signaling in the mPFC biases behavioral responses to punishment-predictive stimuli, rather than reward-predictive cues. Third, in contrast to the well-characterized mPFC-NAc projection, we show that activation of mPFC-dPAG neurons is sufficient to drive place avoidance and defensive behaviors. Fourth, to determine the natural dynamics of individual mPFC neurons, we performed single-cell projection-defined microendoscopic calcium imaging to reveal a robust preferential excitation of mPFC-dPAG, but not mPFC-NAc, neurons to aversive stimuli. Finally, photostimulation of VTA dopamine terminals in the mPFC revealed an increase in signal-to-noise ratio in mPFC-dPAG neuronal activity during the processing of aversive, but not rewarding stimuli. Together, these data unveil the utility of dopamine in the mPFC to effectively filter sensory information in a valence-specific manner.
by Caitlin Miya Vander Weele.
Ph. D. in Neuroscience
Mehta, Mitul Ashok. "Dopaminergic modulation of human cognitive function." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621792.
Full textDecker, Amanda R. "TRPM7 function in zebrafish dopaminergic neurons." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/5927.
Full textYang, Wonsuk. "The bipyridyl herbicide paraquat-induced toxicity in human neuroblastoma SH-SY5Y cells: relevance to dopaminergic pathogenesis." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4384.
Full textKarakuyu, Dilek. "Dopaminergic and serotonergic modulation of working memory." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970180993.
Full textKorotkova, Tatiana. "Hypothalamic modulation of the midbrain dopaminergic system." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968537340.
Full textSt, Onge Jennifer Rose. "Dopaminergic modulation of risk-based decision making." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1313.
Full textHersi, Ali I. "Dopaminergic modulation of the septohippocampal cholinergic system." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40359.
Full textUsing a fimbriaectomy/receptor autoradiography approach, we examined the location of hippocampal dopamine receptors and found that a proportion of dopamine D1-like receptors are likely located on cholinergic terminals in the hippocampus. Moreover, the stimulation of D1-like, but not D2-like, receptors enhanced in vivo hippocampal acetylcholine release, in a phasic manner. The loci for this action is apparently at the level of the cholinergic terminals within the hippocampus.
There are at least two members of the D1-like family of dopamine receptors, namely D1 and D5 subtypes. Owing to the unavailability of selective ligands, we utilized a combined antisense-in vivo dialysis approach in order to ascertain which of these two receptors is involved in modulating hippocampal acetylcholine release. It appears that the D5 receptor subtype is responsible for this function. Interestingly, this is the first evidence of a possible function for the dopamine D5 receptor subtype in the mammalian brain.
This dopaminergic modulation of hippocampal acetylcholine release is preserved as the animal ages. Interestingly, stimulation of D1-like receptors attenuated the memory deficits observed in aged rats in the Morris water maze task. Thus the hippocampal dopamine-acetylcholine interactions likely have a cognitive significance.
Finally, dopamine D1-like receptors were also found in the hippocampal formation of monkey and human brains. It is conceivable, therefore, that dopamine acting via these receptors might serve similar functions in primates as those described above for the rat.
Taken together, the results presented in this thesis provide information about the heteroregulation of the cholinergic synapses in the hippocampus. Most importantly, this work suggests a novel approach to alleviate age-associated memory deficits by stimulating D5 receptors.
Allman, Ava-Ann. "Dopaminergic effects on putative endophenotypes for schizophrenia." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114243.
Full textLa schizophrénie est un trouble mental complexe et dévastateur, considérée comme le résultat des facteurs environnementaux stressant et des troubles du système dopamine (DA). À la recherche de facteurs génétiques, les chercheurs utilisent des phénotypes intermédiaires, des différences cachées dans le fonctionnement de cerveau. La thèse suivante présente trois études examinant la transmission de DA ainsi que les phénotypes intermédiaires putatifs de la schizophrénie.Premièrement, l'effet de la dextroamphétamine (D-amp), un agoniste de DA, sur les tâches des mouvements oculaires a été étudié chez les participants sains. D-amp a réduit de la proportion des erreurs sur la tâche antisaccade mais n'a eu aucun effet sur la tâche saccade prédictive. On peut donc conclure que les taux d'erreurs chez les antisaccades, un phénotype intermédiaire putatif, ont été réduit par agoniste dopaminergiques. Nous avons ensuite examiné l'effet d'un autre agoniste de DA, le méthylphénidate (MPH), sur les tâches oculomotrices. Le MPH n'avait aucun effet sur la performance de l'antisaccade. Il augmentait la proportion des saccades prédictives uniquement chez des conditions de choix d'horaire prévisibles ; ceci appuie l'hypothèse de l'effet du MPH sur les fonctions de synchronisation. Le médicament améliore également une poursuite lisse et un phénotype intermédiaire oculomoteur putatif. Les différences entre les effets de la D-amp et le MPH sont considérées en termes de différences dans l'action des médications. Finalement, la réactivité du système DA a été évaluée avec l'aide d'une tâche de stress psychosocial chez des individus avec des risques élevés de schizophrénie et des participants sains. La DA au repos ainsi que la libération de la DA ont été quantifié avec [11]C raclopride et la tomographie par émission de positions (TEP) en utilisant la tâche du stress d'imagerie de Montréal. Ont été également évalué la réactivité de l'axe HPA et le volume l'hippocampe. Les individus avec des risques élevés avaient un pouvoir de fixation nettement plus faible que chez les participants sains, ce qui suggère un accroissement des niveaux de DA endogènes, cohérent avec les résultats chez les patients. Le stress induit par la libération de la DA ne différaient pas entre les groupes. La libération de la DA a été corrélé négativement avec la libération de cortisol. Même si le volume d'hippocampique a corrélé avec la libération de cortisol, elle n'a pas eu le même effet avec la libération de la DA. Les résultats indiquent un rôle de la DA dans les tâches des mouvements oculaires qui sont caractérisés comme étant des phénotypes intermédiaires putatifs pour la schizophrénie et suggèrent également que la dérégulation du système de la DA au repos pourrait être en soi un phénotype intermédiaire de la maladie.
Love, Rebecca Margaret. "Improving the survival of embryonic dopaminergic neurons." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343277.
Full textMcAfee, Ghia. "Smoking and brain dopaminergic neurochemistry / Ghia McAfee." Thesis, North-West University, 2004. http://hdl.handle.net/10394/590.
Full textThesis (Ph.D. (Pharmaceutical Chemistry))--North-West University, Potchefstroom Campus, 2005.
Chowdhury, R. "Dopaminergic enhancement of cognition in old age." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1388281/.
Full textBarrie, Elizabeth Stofko. "Genetic Factors Regulating Expression of Dopaminergic Genes." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1406388433.
Full textEdman, Linda C. "Chemokines and their role in dopaminergic development." Stockholm : Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-688-0/.
Full textRizvi, Nisha. "NOVEL DOPAMINERGIC SIGNALING MODULATING HIPPOCAMPAL SYNAPTIC TRANSMISSION." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1082.
Full textTuathaigh, Colm O. "Dopaminergic involvement in stimulus selection : a behavioural study." Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/31325.
Full textTripanichkul, Wanida 1962. "Associations between glia and sprouting of dopaminergic axons." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/7630.
Full textCanales, Juan Jose. "Behavioural correlates of dopaminergic manipulations of the striatum." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364066.
Full textLivingstone, Phil. "Nicotinic modulation of dopaminergic signalling in the PFC." Thesis, University of Bath, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528111.
Full textPöltl, Dominik [Verfasser]. "Degeneration mechanisms in human dopaminergic neurons / Dominik Pöltl." Konstanz : Bibliothek der Universität Konstanz, 2012. http://d-nb.info/1025226135/34.
Full textFoy, Catherine Mary Louise. "The non dopaminergic neuropharmacology of idiopathic Parkinson's disease." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392537.
Full textKillcross, 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.
Full textKeeler, Joshua Finn. "Instrumental response sequencing : dopaminergic modulation and behavioural control." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648582.
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