Bibliographies thématiques / Dopaminergici

Littérature scientifique sur le sujet « Dopaminergici »

Auteur : Grafiati
Publié le 10 mars 2023

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Articles de revues sur le sujet "Dopaminergici"

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Colao, Annamaria, et Renata Simona Auriemma. « Iperprolattinemia, farmaci dopaminergici e valvulopatie : vero o falso ? » L'Endocrinologo 13, no 3 (juin 2012) : 127–31. http://dx.doi.org/10.1007/bf03345965.

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Frazzitta, Giuseppe. « La malattia di Parkinson : fi siopatologia, cure farmacologiche, multidisciplinarietà ». PNEI REVIEW, no 2 (novembre 2022) : 9–19. http://dx.doi.org/10.3280/pnei2022-002002.

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I Parkinsonismi sono un gruppo di disturbi del movimento classificate in forme secondarie e degenerative. La malattia di Parkinson è una forma degenerativa di Parkinsonismo dovuta alla degenerazione della sostanza nigra e alla perdita dei suoi neuroni dopaminergici. La dopamina da essi prodotta ha una funzione di modulazione dell'attività dei nuclei della base. La perdita di tale modulazione porta a una riduzione del movimento con aumento della rigidità, lentezza e parziale perdita di alcuni movimenti automatici: i riflessi posturali, la deambu- lazione e il pendolarismo. La L-Dopa a partire dalla fine degli anni '60 del Novecento ha permesso di curare questi pazienti con miglioramento della rigidità e della lentezza. La breve emivita di questo farmaco ha richiesto lo sviluppo di altre molecole che ne permettessero il prolungamento dell'azione. Purtroppo non sempre tali nuovi farmaci sono risultati efficaci o hanno causato importanti effetti collaterali. La riabilitazione si è rivelata essere efficace nel migliorare gli aspetti motori della malattia e nel migliorare la qualità di vita dei pazienti. Per tale ragione un approccio multidisciplinare e integrato è adesso consigliato come miglior trattamento dei pazienti con malattia di Parkinson.
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Dzoljic, Eleonora, Zorica Nesic, Radan Stojanovic, Nevena Divac, Zoran Todorovic, Sonja Vuckovic, Vladimir Kostic et Milica Prostran. « Azotni oksid, neurodegeneracija i Parkinsonova bolest ». Vojnosanitetski pregled 62, no 10 (2005) : 751–56. http://dx.doi.org/10.2298/vsp0510751d.

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<zakljucak> Brojni rezultati velikih studija pokazuju znacajnu ulogu NO u kaskadi dogadjaja koji dovode do smrti dopaminergickih neurona. Zna se da MPTP uzrokuje neurotoksicnost putem NO sintetisanog pomocu nNOS, ostecujuci primarno dopaminergicka vlakna i zavrsetke u strijatumu, dok NO stvoren uz pomoc iNOS deluje prvenstveno na tela dopaminergickih neurona u pars compacta substantia nigra. Ostecenje uzrokovano NO iz nNOS moze sluziti kao katalizator aktivacije iNOS i glioze. Slican sled dogadjaja moze se primeniti na ostecenje dopaminergickih neurona kod ljudi, bilo usled idiopatske PB ili usled intoksikacije MPTP. Znacaj ovih otkrica je ne samo u osvetljavanju cinioca koji ucestvuju u progresiji neurodegeneracije i PB vec i u upucivanju na nove terapijske mogucnosti.
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Prysiazhniuk, A. I., M. P. Rudyk, M. Chervinska, T. V. Dovbynchuk, L. M. Skivka et G. M. Tolstanova. « Role of peripheral dopaminergic system in the pathogenesis of experimental colitis in rats ». Ukrainian Biochemical Journal 89, no 4 (21 juillet 2017) : 56–67. http://dx.doi.org/10.15407/ubj89.04.056.

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Werner, Felix-Martin, et Rafael Coveñas. « Comparison of Mono-dopaminergic and Multi-target Pharmacotherapies in Primary Parkinson Syndrome and Assessment Tools to Evaluate Motor and Non-motor Symptoms ». Current Drug Therapy 14, no 2 (27 août 2019) : 124–34. http://dx.doi.org/10.2174/1574885513666181115104137.

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Background:Primary Parkinson syndrome is mostly treated by dopaminergic drugs, while the progression of the disease is not altered. Some non-dopaminergic are available, which are administered only after the Parkinsonian symptoms get worse.Objective:The objective of this review is to give basic results in order to compare a dopaminergic and non-dopaminergic pharmacotherapy in Parkinson’s disease and to control whether the add-on pharmacotherapy with non-dopaminergic drugs can inhibit the progression of the disease.Methods:In primary Parkinson syndrome, the altered activity of classical neurotransmitters and neuropeptides in the extrapyramidal system is summarized and up-dated. Anatomical studies on neural networks in the basal ganglia are mentioned. The direct, motor facilitatory pathway (D1 dopaminergic neurons) from the substantia nigra to the thalamus, via the internal globus pallidus, and the indirect, motor inhibitory pathway via D2 dopaminergic neurons have been considered. These established anatomical pathways have been brought in line with the neural interactions derived from neurotransmitter balances or imbalances. Besides, preclinical and clinical studies of effective non-dopaminergic anti-Parkinsonian drugs are reviewed.Results:It can be hypothesized that glutamatergic neurons enhance dopamine deficiency in the substantia nigra and putamen through an increased presynaptic inhibition mediated by NMDA receptors. In the putamen, 5-HT2A serotonergic neurons counteract D2 dopaminergic neurons and A2A adenosine neurons antagonize D2 dopaminergic neurons by activating glutamatergic neurons, which presynaptically inhibit via subtype 5 of metabotropic glutamatergic receptors, D2 dopaminergic neurons. In the extrapyramidal system, an up-dated neural network, which harmonizes established anatomical pathways with derived neural interactions, is presented. In Parkinson’s disease, a question should be answered, whether a combination of dopaminergic and non-dopaminergic drugs can promote an increased motor and non-motor functioning.Conclusion:A mono-target pharmacotherapy (using only dopaminergic drugs) and a multi-target pharmacotherapy (i.e. by combining dopaminergic and non-dopaminergic drugs) are compared. The alternate administration of dopaminergic and non-dopaminergic anti-Parkinsonian drugs, administered at different times during the day, must be tested in order to inhibit the progression of the disease. Assessment tools can be used to evaluate motor and cognitive functions. Moreover, imaging examination techniques can be also applied to control the course of the disease.
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Fernández-López, Blanca, Daniel Romaus-Sanjurjo, María Eugenia Cornide-Petronio, Sonia Gómez-Fernández, Antón Barreiro-Iglesias et María Celina Rodicio. « Full Anatomical Recovery of the Dopaminergic System after a Complete Spinal Cord Injury in Lampreys ». Neural Plasticity 2015 (2015) : 1–10. http://dx.doi.org/10.1155/2015/350750.

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Following a spinal injury, lampreys at first are paralyzed below the level of transection. However, they recover locomotion after several weeks, and this is accompanied by the regeneration of descending axons from the brain and the production of new neurons in the spinal cord. Here, we aimed to analyse the changes in the dopaminergic system of the sea lamprey after a complete spinal transection by studying the changes in dopaminergic cell numbers and dopaminergic innervation in the spinal cord. Changes in the expression of the D2 receptor were also studied. We report the full anatomical regeneration of the dopaminergic system after an initial decrease in the number of dopaminergic cells and fibres. Numbers of dopaminergic cells were recovered rostrally and caudally to the site of injury. Quantification of dopaminergic profiles revealed the full recovery of the dopaminergic innervation of the spinal cord rostral and caudal to the site of injury. Interestingly, no changes in the expression of the D2 receptor were observed at time points in which a reduced dopaminergic innervation of the spinal cord was observed. Our observations reveal that in lampreys a spinal cord injury is followed by the full anatomical recovery of the dopaminergic system.
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Niu, Shiba, Weibo Shi, Yingmin Li, Shanyong Yi, Yang Li, Xia Liu, Bin Cong et Guanglong He. « Endoplasmic Reticulum Stress Is Associated with the Mesencephalic Dopaminergic Neuron Injury in Stressed Rats ». Analytical Cellular Pathology 2021 (8 septembre 2021) : 1–9. http://dx.doi.org/10.1155/2021/7852710.

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An increasing number of people are in a state of stress due to social and psychological pressures, which may result in mental disorders. Previous studies indicated that mesencephalic dopaminergic neurons are associated with not only reward-related behaviors but also with stress-induced mental disorders. To explore the effect of stress on dopaminergic neuron and potential mechanism, we established stressed rat models of different time durations and observed pathological changes in dopaminergic neurons of the ventral tegmental area (VTA) through HE and thionine staining. Immunohistochemistry coupled with microscopy-based multicolor tissue cytometry (MMTC) was employed to investigate the number changes of dopaminergic neurons. Double immunofluorescence labelling was used to investigate expression changes of endoplasmic reticulum stress (ERS) protein GRP78 and CHOP in dopaminergic neurons. Our results showed that prolonged stress led to pathological alteration in dopaminergic neurons of VTA, such as missing of Nissl bodies and pyknosis in dopaminergic neurons. Immunohistochemistry with MMTC indicated that chronic stress exposure resulted in a significant decrease in dopaminergic neurons. Double immunofluorescence labelling showed that the endoplasmic reticulum stress protein took part in the injury of dopaminergic neurons. Taken together, these results indicated the involvement of ERS in mesencephalic dopaminergic neuron injury induced by stress exposure.
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Barbanti, Piero, Cinzia Aurilia, Gabriella Egeo, Luisa Fofi, Fiorella Guadagni et Patrizia Ferroni. « Dopaminergic symptoms in migraine : A cross-sectional study on 1148 consecutive headache center-based patients ». Cephalalgia 40, no 11 (2 juin 2020) : 1168–76. http://dx.doi.org/10.1177/0333102420929023.

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Background Dopaminergic symptoms may be extremely pronounced in some migraine patients during the attack, representing a major source of disability. Objectives We aimed to carefully characterize the clinical picture of migraine patients with dopaminergic symptoms in a large patients’ population as a putative migraine endophenotype, allowing more precise disease management, treatment and outcome prediction. Methods We screened 1148 consecutive tertiary care episodic and chronic migraine patients with face-to-face interviews collecting thorough data on lifestyle, socio-demographic factors, and clinical migraine features. Results We identified 374 patients with migraine with dopaminergic symptoms (32.6%). The most frequent dopaminergic symptom was yawning followed by somnolence, nausea, vomiting, fatigue, mood changes and diuresis. Migraine patients with dopaminergic symptoms had longer attack duration (OR: 1.82; 95% CI: 1.41–2.36, p < 0.0001), more frequent osmophobia (OR: 2.01; 95% CI: 1.50–2.69, p < 0.0001), allodynia (OR: 1.43; 95% CI: 1.10–1.85, p = 0.0071) and unilateral cranial autonomic symptoms (OR: 1.31; 95% CI: 1.01–1.68, p = 0.045), but used less preventative treatments (OR: 0.74; 95% CI: 0.57–0.98, p = 0.033) than patients without dopaminergic symptoms. Conclusions Migraine patients with dopaminergic symptoms are characterized by a full-blown, more disabling migraine. Dopaminergic system modulation should be carefully considered in individuals with migraine with dopaminergic symptoms for both acute and preventative treatments in future ad hoc designed studies.
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Gale, Samuel D., et David J. Perkel. « Physiological Properties of Zebra Finch Ventral Tegmental Area and Substantia Nigra Pars Compacta Neurons ». Journal of Neurophysiology 96, no 5 (novembre 2006) : 2295–306. http://dx.doi.org/10.1152/jn.01040.2005.

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The neurotransmitter dopamine plays important roles in motor control, learning, and motivation in mammals and probably other animals as well. The strong dopaminergic projection to striatal regions and more moderate dopaminergic projections to other regions of the telencephalon predominantly arise from midbrain dopaminergic neurons in the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA). Homologous dopaminergic cell groups in songbirds project anatomically in a manner that may allow dopamine to influence song learning or song production. The electrophysiological properties of SNc and VTA neurons have not previously been studied in birds. Here we used whole cell recordings in brain slices in combination with tyrosine-hydroxylase immunolabeling as a marker of dopaminergic neurons to determine electrophysiological and pharmacological properties of dopaminergic and nondopaminergic neurons in the zebra finch SNc and VTA. Our results show that zebra finch dopaminergic neurons possess physiological properties very similar to those of mammalian dopaminergic neurons, including broad action potentials, calcium- and apamin-sensitive membrane-potential oscillations underlying pacemaker firing, powerful spike-frequency adaptation, and autoinhibition via D2 dopamine receptors. Moreover, the zebra finch SNc and VTA also contain nondopaminergic neurons with similarities (fast-firing, inhibition by the μ-opioid receptor agonist [d-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO)) and differences (strong h-current that contributes to spontaneous firing) compared with GABAergic neurons in the mammalian SNc and VTA. Our results provide insight into the intrinsic membrane properties that regulate the activity of dopaminergic neurons in songbirds and add to strong evidence for anatomical, physiological, and functional similarities between the dopaminergic systems of mammals and birds.
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Wasel, Ola, et Jennifer L. Freeman. « Chemical and Genetic Zebrafish Models to Define Mechanisms of and Treatments for Dopaminergic Neurodegeneration ». International Journal of Molecular Sciences 21, no 17 (20 août 2020) : 5981. http://dx.doi.org/10.3390/ijms21175981.

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The zebrafish (Danio rerio) is routinely used in biological studies as a vertebrate model system that provides unique strengths allowing applications in studies of neurodevelopmental and neurodegenerative diseases. One specific advantage is that the neurotransmitter systems are highly conserved throughout vertebrate evolution, including between zebrafish and humans. Disruption of the dopaminergic signaling pathway is linked to multiple neurological disorders. One of the most common is Parkinson’s disease, a neurodegenerative disease associated with the loss of dopaminergic neurons, among other neuropathological characteristics. In this review, the development of the zebrafish’s dopaminergic system, focusing on genetic control of the dopaminergic system, is detailed. Second, neurotoxicant models used to study dopaminergic neuronal loss, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the pesticides paraquat and rotenone, and 6-hydroxydopamine (6-OHDA), are described. Next, zebrafish genetic knockdown models of dj1, pink1, and prkn established for investigating mechanisms of Parkinson’s disease are discussed. Chemical modulators of the dopaminergic system are also highlighted to showcase the applicability of the zebrafish to identify mechanisms and treatments for neurodegenerative diseases such as Parkinson’s disease associated with the dopaminergic system.
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Thèses sur le sujet "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.

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1. Introduzione I neuroni dopaminergici (DA) della substantia nigra pars compacta (SNc) sono tra i più studiati nel sistema nervoso centrale per la loro implicazione nella malattia del Parkinson. Essi presentano un ampio corredo di correnti voltaggio-dipendenti, tra le quali emerge una tipica corrente attivata da iperpolarizzazione, la Ih. Diversamente dalla maggior parte delle cellule nervose, i neuroni dopaminergici della SNc presentano una attività spontanea regolare dopo isolamento o riduzione degli input sinaptici, e non è, quindi, sorprendente che numerosi lavori abbiano indagato il ruolo della Ih nell'attività spontanea. Tuttavia il ruolo della Ih non è stato ancora ben compreso, dal momento che il blocco di questa corrente non sembra comportare nessuna alterazione significativa della frequenza di scarica. Abbiamo, allora, riesaminato il problema studiando la corrente h, in fette sottili di cervello, in condizioni sperimentali che si differenziano dalla maggior parte degli studi precedenti per tre aspetti fondamentali: i) abbiamo utilizzato topi transgenici che esprimono una proteina reporter (GFP) sotto il promotore tirosina idrossilasi (TH), per identificare i neuroni DA della SNc; ii) abbiamo effettuato le registrazioni elettrofisiologiche a 37°C; iii) abbiamo eseguito la maggior parte degli esperimenti in condizioni di patch perforato al fine di lasciare inalterato l’ambiente fisiologico intracellulare. 2. Risultati Il nostro primo obiettivo è stato quello di effettuare un'analisi dettagliata della dipendenza della cinetica e dell’ampiezza della Ih dalla temperatura. Il protocollo di attivazione della corrente h prevedeva una serie di comandi iperpolarizzanti della durata di 4s e le registrazioni erano effettuate a 27°C e 37°C. Abbiamo calcolato che il coefficiente di temperatura (Q10) per la variazione di ampiezza della corrente h è pari 3,73, mentre i valori di Q10 relativi alle velocità di attivazione e deattivazione sono rispettivamente pari a 10,8 e 3,17. Il V50 è di -94,9 ± 1,07 mV a 27°C (n = 13) e -84,2 ± 1,31 mV a 37°C (n = 18). Abbiamo, successivamente, esaminato la modulazione da parte dei nucleotidi ciclici in condizioni di patch perforato a 37°C, in presenza di forskolina (10 μM), un attivatore della adenilato ciclasi, e IBMX (0.1 mM), un inibitore delle fosfodiesterasi, i quali, insieme, inducono un aumento della concentrazione intracellulare di adenosina monofosfato ciclico (cAMP). In queste condizioni abbiamo registrato un aumento dell'ampiezza Ih (da -178,53 ± 23,48 pA in condizioni di controllo a -227,01 ± 34,17 pA con forskolina a -130 mV, n = 8), uno spostamento del V50 di + 4,80 ± 0,68 mV (n = 8) e una riduzione delle costanti di tempo di attivazione di circa il 25%. Dato che questa modulazione è il risultato di un’interazione diretta del cAMP con il canale, abbiamo studiato gli effetti sulla Ih di diversi neurotrasmettitori accoppiati a proteine Gi o Gs, in particolare abbiamo testato la dopamina, la serotonina (5-HT) e la noradrenalina (NA). Il quinpirolo, un agonista dei recettori dopaminergici D2 (30 μM, dopo 3 minuti di applicazione nel bagno), ha indotto una diminuzione dell'ampiezza della Ih del 15% a -130 mV (n = 6), mentre il sulpiride, un antagonista dei recettori dopaminergici D2 (20 μM), ne ha determinato un aumento (n = 5). L'effetto sulla Ih della 5HT (100 μM), dopo 3 minuti di applicazione nel bagno, è stato una riduzione dell’ampiezza del 20% (n = 5); al contrario, l'applicazione nel bagno della NA (100 μM), ne ha indotto un aumento di circa il 12% (n = 8). Infine, abbiamo analizzato il ruolo della corrente h sull’autoritmicità. L'ivabradina (10 μM), bloccante del Ih, ha determinato una marcata iperpolarizzazione (circa -10 mV), che di fatto ha silenziato le cellule; tuttavia, questo effetto sull’attività spontanea era indiretto, poiché se la membrana era ripolarizzata, l’autoritmicità si ripristinava. 3. Conclusioni Gli studi eseguiti a temperatura ambiente sul ruolo e le proprietà della corrente h nei neuroni dopaminergici della SNc sono scarsamente informativi perché, in queste condizioni sperimentali, la corrente è sottovalutato in ampiezza, velocità e, in ultima analisi, nella sua capacità di svolgere alcun ruolo a potenziali fisiologici. Le registrazioni elettrofisiologiche a 37°C, invece, restituiscono un profilo più accurato e veritiero della Ih. La modulazione della corrente h ad opera di sistemi a secondo messaggero, un processo scarsamente esplorato nei neuroni dopaminergici della SNc, sembra essere rilevante, e suggerisce l'esistenza di diversi pathways importanti per il controllo dell’eccitabilità neuronale. La corrente h è, in ultima analisi, molto importante nell’autorimicità perché stabilizza il potenziale di membrana di riposo dei neuroni dopaminergici della SNc in uno stato depolarizzato, ma non ricopre un ruolo di principale nell’attività pacemaker. Questi risultati sono interessanti perché aprono nuove prospettive sul ruolo del canale HCN nei neuroni dopaminergici della substantia nigra pars compacta.
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GIUSTIZIERI, 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.

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L’inibizione presinaptica è un meccanismo di modulazione sinaptica comunemente osservato nelle sinapsi del sistema nervoso centrale e periferico. Questo processo inizia in risposta all’attivazione di un’ampia varietà di recettori presinaptici e porta ad una riduzione della probabilità di fusione delle vescicole con la membrana del terminale sinaptico. Uno dei più comuni meccanismi d’azione consiste nell’inibizione dei canali del calcio voltaggio dipendenti (VDCCs) localizzati nei bottoni presinaptici. Tuttavia, esistono altre forme di inibizione presinaptica con meccanismi che coinvolgono direttamente la machinery di rilascio vescicolare. In questa tesi ho studiato il meccanismo di inibizione presinaptica mediata dal recettore metabotropico del glutammato del tipo III (mGluRs) e dal recettore GABAB nella trasmissione GABAergica dei neuroni dopaminergici della substantia nigra pars compacta (SNc) di ratto. L’AP-4 (100 μM), agonista selettivo del recettore metabotropico del glutammato del tipo III, e il baclofen (10 μM), agonista selettivo del recettore GABAB, riducono reversibilmente la frequenza delle correnti spontanee inibitorie post-sinaptiche (sIPSCs) rispettivamente del 48.5 ± 3.7 % e del 83.6 ± 2.3 % rispetto al controllo, senza avere alcun effetto sull’ampiezza della corrente. L’AP-4, non deprime la frequenza delle correnti inibitorie miniature post-sinaptiche (mIPSCs), registrate in tetrodotossina (TTX, 1 μM) e cadmio (100 μM), mentre è in grado di ridurre la frequenza delle mIPSCs del 75.3 ± 2.8 % rispetto al controllo, in presenza di TTX (1 μM) e bario (1 mM). Al contrario, il baclofen riduce la frequenza delle mIPSCs sia in cadmio (70.0 ± 6.7 % del controllo) sia in bario (52.3 ± 2.9 % del controllo). In TTX e ionomicina (2 μM), il baclofen riduce significativamente la frequenza delle mIPSCs del 71.8 ± 6.9 % del controllo, mentre l’AP-4 non ha effetto. In maniera simile, in presenza di TTX e α-latrotossina (α-LTX, 0.3 nM), la frequenza delle mIPSCs è diminuita del 64.5 ± 4.8 % del controllo dal baclofen, mentre mantiene gli stessi valori in presenza di AP-4. Infine, in continua presenza di baclofen, l’AP-4 non causa un ulteriore riduzione della frequenza delle sIPSCs. La conclusione di questi studi è che i recettori metabotropici del glutammato del tipo III deprimono il rilascio di GABA dai neuroni dopaminergici della SNc , attraverso l’inibizione dei VDCC, mentre i recettori presinaptici GABAB coinvolgono direttamente il rilascio vescicolare del neurotrasmettitore. Inoltre questi due diversi meccanismi di inibizione pre-sinaptica coesistono nello stesso terminale sinaptico. Questa caratterizzazione fornisce nuove conoscenze sul ruolo di questi recettori presinaptici nello studio della fisiologia della substantia nigra e nel loro potenziale uso come target nel trattamento farmacologico di malattie neurodegenerative come il morbo di Parkinson.
Presynaptic 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.
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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.

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The mesolimbic dopaminergic pathway plays an important role in the genesis of emotional arousal and behavioral activation in response to stimuli that provide a reward. This neural circuitry is also active in the early stages of learning and stabilization of addictive behavior due to substances abuse. Isolated animals have a different sensitivity to natural or artificial reinforcers. Accordingly, experimental evidences suggest that exposure to stress can deeply modify eating behavior. In light of these evidences the aim of this study was to investigate the influence of a chronic stress, like social isolation at weaning, on the sensitivity of mesocorticolimbic dopaminergic neurons to anticipation and consumption of food. Rats have been food restricted using a protocol that consists in training the animals to consume their meal for only two hours for day. Using vertical microdialysis, extracellular concentrations of dopamine in response to anticipation and consumption of food were measured both in the mPFC and the NAC. In PFC of GH rats extracellular DA increased (+180%) 80 minutes before food presentation showing the maximal increase (+350%) during food intake. On the contrary, in the NAc of GH rats no significant changes were observed. In SI animals trained to food restriction the increase in mPFC DA output observed in GH animals was completely blunted, while, in the NAc, 40 min before the presentation of the food, a significant increase in extracellular concentrations of DA was observed. Our results show that exposure to chronic stress modified the response of mesocortico-limbic dopaminergic neurons to an enjoyable stimulus and suggest that these changes might be important to explain the greater sensitivity to abuse that is observed in individuals subjected to stressful stimuli. This underlying alteration in brain function might be a crucial mechanism that predisposes individuals to impulsive behavior and increases the risk of developing addiction.
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CUCCHIARONI, 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.

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E’ sempre più accettata l’ipotesi secondo cui le malattie neurodegenerative come il morbo di Parkinson siano di origine multifattoriale (“multiple hit hypothesis”), cioè siano causate dalla concomitante o ripetitiva presenza di diversi fattori che cooperano alla morte cellulare. Tra questi quelli ambientali occupano un posto rilevante. Sebbene una grande varietà di processi neurologici potrebbero essere influenzati da neurotossine ambientali, il sistema dopaminergico sembra essere quello più colpito. Negli ultimi 10 anni si è rivolta sempre maggiore attenzione alla L-BMAA (L-β-N-methylamino-L-alanine), un aminoacido non proteico trovato nei semi della Cycas micronesica, che sembra essere alla base dell’ “ALS-PDC complex”, una sindrome complessa caratterizzata da sintomatologie cliniche tipiche della sclerosi laterale amiotrofica (SLA), del morbo di Parkinson e dell’Alzheimer. Recenti scoperte hanno dimostrato che questa tossina viene prodotta da una grande varietà di cianobatteri del genere Nostoc presenti in tutto il mondo. Pertanto, potenzialmente, tutta la popolazione umana potrebbe essere esposta a tale sostanza. Ciò potrebbe determinare il suo accumulo nell’organismo, sia in forma libera che legata alle proteine, da cui verrebbe poi rilasciata lentamente durante il catabolismo proteico. Sulla base di queste considerazioni abbiamo voluto analizzare gli effetti di questo aminoacido sulle cellule dopaminergiche della SNc da un punto di vista elettrofisiologico, farmacologico, morfologico e tossicologico. La BMAA (3 mM, 10 psi 1.0 s) causa una depolarizzazione dei neuroni dopaminergici della SNc inducendo una corrente entrante (media = 454.48 ± 34.65, n = 73) e aumenti transienti della concentrazione di calcio intracellulare (R medio = 0.368 ± 0.062, n = 13). Questi effetti sono mediati prevalentemente dall’attivazione dei recettori metabotropici del glutammato di gruppo I (mGluR1), in quanto vengono ridotti reversibilmente dall’antagonista selettivo, CPCCOEt (100 μM) (corrente: 41.56 ± 3.61 % del controllo, n = 24; calcio: 28.43 ± 5.96 % del controllo, n = 7). La corrente, ma non il calcio, indotta dalla BMAA è ridotta in piccola parte dal CNQX (10 μM) (corrente: 93,09 ± 1,97 % del controllo, n = 24; calcio: 100.17 ± 9.93 % del controllo, n=6), antagonista competitivo dei recettori AMPA. Nelle cellule dopaminergiche della SNc gli aumenti di calcio indotti dall’attivazione dei recettori mGluR1 sono mediati dai canali SOCs/TRPC. Infatti, sia le correnti entranti che le variazioni di calcio intracellulare indotte dalla BMAA sono ridotte dagli antagonisti di tali canali, SKF 96365 (100 μM) (corrente: 42.125 ± 4.35 % del controllo, n = 8; calcio: 43.57 ± 7.9 % del controllo, n = 7) e Ruthenium Red (20 μM) (corrente: 27.05 ± 8.3 % del controllo, n = 6). Inoltre, nonostante la BMAA in presenza di carbonato presenti una struttura chimica simile a quella dell’acido glutammico, essa non viene ricaptata dalla cellule dopaminergiche attraverso il trasportatore degli aminoacidi eccitatori EAAT. E’ interessante notare che negli interneuroni GABAergici della SNc la BMAA attiva i recettori AMPA, ma non quelli metabotropici, senza indurre variazioni della concentrazione del calcio intracellulare. In queste cellule, tuttavia, l’agonista selettivo degli mGluR1, il DHPG (30 μM), evoca correnti entranti, a dimostrazione della presenza degli mGluR1 sugli interneuroni GABAergici. A conferma della sua potenziale tossicità, esposizioni prolungate di fettine mesencefaliche (12, 20 e 30 minuti) alla BMAA inducono cambiamenti irreversibili su numerose proprietà cellulari. Tali modificazioni sono accompagnate dal rilascio massivo del citocromo C (Cyt C) nel citoplasma delle cellule dopaminergiche che viene completamente bloccato dall’aggiunta, nel mezzo di perfusione, di antagonisti dei recettori mGluR1 e AMPA. I dati che ho riportato in questa tesi forniscono una chiara e plausibile dimostrazione di come la BMAA può essere tossica verso le cellule dopaminergiche della SNc, causando i sintomi neurologici della malattia di Parkinson.
It 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.
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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.

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Oxytocin, the neurohypophyseal hormone well-known for its hormonal role in lactation and parturition, also exerts a wide range of effects acting in the Central Nervous System as a neuromodulator or neurotransmitter. An increasing number of experimental studies have suggested that, in rodents, central oxytocin exerts also a modulatory role on locomotor activity, but little is known about the cerebral areas in which oxytocin might act to produce this effect. The substantia nigra, a mesencephalic structure which is part of the basal ganglia, a group of interconnected nuclei involved in motor and non-motor functions, receives oxytocinergic projections from the parvocellular compartment of the paraventricular nucleus of the hypothalamus. Moreover, oxytocinergic receptors and oxytocin receptor messenger RNA have been shown to be present in human and rat substantia nigra, respectively. Furthermore, it has been demonstrated that a significant decrease in the number of oxytocin-immunoreactive neurons occurs in the paraventricular nucleus of patients suffering from Parkinson’s Disease, a progressive neurodegenerative movement disorder characterised by the degeneration of the cell bodies of nigrostriatal dopaminergic neurons projecting to the dorsal striatum. In order to investigate the role of nigral oxytocin in locomotor activity, a combined approach comprehensive of immunohistochemical, behavioural and lesion studies, has been used in male rats. First, the effect on locomotor activity of low and high doses of oxytocin, given intraperitoneally or into the substantia nigra, and of d(CH2)5Tyr(Me)2-Orn8-vasotocin, a selective oxytocin receptor antagonist, given into the lateral ventricles or into the substantia nigra, were studied in male rats habituated to the experimental conditions in order to avoid novelty-induced behavioural effects. Second, the presence of nigral oxytocinergic fibres and their localization with respect to nigral neurons immunoreactive for tyrosine hydroxylase (TH) (a marker of dopaminergic neurons) was investigated by immunohistochemistry. Finally, the effect on spontaneous locomotor activity of the bilateral injection into the substantia nigra of oxytocin-saporin (OXY-SAP), a recently discovered neurotoxin that specifically destroys neurons presenting oxytocinergic receptors on their surface, was studied in relation to the modifications induced in the dopaminergic, glutamatergic and GABAergic systems, assessed by immunohistochemistry using antibodies against TH, vesicular glutamate transporters (VGluT1, VGluT2 and VGluT3) and glutamate decarboxylase (GAD). Together, the results of the above experiments with oxytocin and d(CH2)5Tyr(Me)2-Orn8-vasotocin and those with OXY-SAP, which revealed the existence of a correlation between the changes in locomotor activity found in OXY-SAP-treated rats and the extent of the changes in nigral TH, VGluT1, VGluT2 and VGluT3 immunoreactivities measured at 28 days after OXY-SAP injection, provide support for a modulatory role of oxytocin on locomotor activity at the level of the substantia nigra.
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ESPA, 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.

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Pramipexole (PPX) is a dopamine (DA) D3 and D2 receptors agonist widely used alone or in combination with levodopa as Dopamine Replacement Therapy in Parkinson’s disease. In clinical and preclinical studies, PPX improved motor deficits, this evidence led to lowering daily dose of levodopa, delaying the motor side effects associated with its use. Recently, PPX administration has been associated to the development of addictive-like behaviors related to the DA Dysregulation Syndrome, particularly in a subpopulation of treated patients, characterized by impulsive-compulsive personality traits as well as previous addiction’s experience. Based on these evidences, the aim of this study was twofold: first to investigate the pharmacological action of PPX, using a unilateral model of Parkinson’s disease in which 6-OHDA was injected in the medial forebrain bundle. After two weeks, we tested in primed and naive rats, the ability of three different doses of PPX (0,035; 0,1 and 0,35 mg/kg s.c.), to induce contralateral turning behavior as well c-fos expression after pretreatment of DA D1 antagonist SCH 39166. Next, we checked the ability of PPX to induce contralateral rotations after D2 (eticlopride) and D3 (S33084) DA antagonist pretreatment. In order to investigate the role of PPX (0,05 mg/kg s.c.) in behavioral sensitization, we tested its effect with S33084 pretreatment in levodopa sensitized rats. Second, we assessed the correlation between PPX treatment, Parkinson’s disease and the onset of DA Dysregulation Syndrome on Conditioned Place Preference (CPP) paradigm. To do this, 6-OHDA was injected bilaterally in DA striatal terminals, in three different strains of rat: the addiction prone Lewis (LEW), the addiction resistant Fisher 344 (F344) inbred strains, and the Sprague Dawley (SD) outbred strain. Furthermore, to test its rewarding properties, PPX was directly infused in the nucleus accumbens shell (NAc), a DA mesolimbic region known to be involved in the rewarding effects of drugs of abuse, in healthy rats belonging to the above mentioned strains. We discovered that in primed rats, PPX (0,35 mg/kg s.c.) induced turning behavior that was increased by SCH 39166 pretreatment (0,1 mg/kg s.c.). No effect was seen in naive rats both for turning behavior and c-fos expression. D2 receptors antagonist eticlopride (0,1 mg/kg s.c.) reduced PPX-induced turning behavior more than D3 receptors antagonist S33084 (0,5 mg/kg s.c.), also a previous levodopa sensitization increased PPX-induced turning behavior on its first administration. This suggests that PPX’s action could be related to D2 stimulation, and it seems to require a previous D1/D2 stimulation to observe a behavioral outcome. PPX (1 mg/kg s.c.) was able to induce a significant CPP in SD and LEW lesioned rats but not in F344 and control rats, and the persistence of preference was stronger in LEW than in SD rats. When injected into the NAc shell, PPX (5 μg/0.5 μl) induced CPP in all rat strains, but the persistence of its effect was more strong in LEW compared to SD and F344 rats. These results suggest that the parkinsonian state might be more sensitive to the rewarding properties of PPX, which do not seem entirely influenced by phenotype.
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CAVALLERI, 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.

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La degenerazione dei neuroni dopaminergici (DA) del mesencefalo ventrale è considerata uno dei segni distintivi della malattia di Parkinson (PD) e del Parkinsonismo. La loro suscettibilità al danno e la loro adattabilità e plasticità sono state inizialmente studiate in modelli animali per comprendere i meccanismi cellulari e molecolari e l'azione delle terapie farmacologiche. La recente introduzione della tecnologia delle cellule staminali pluripotenti indotte umane (iPSCs) e lo sviluppo di protocolli per la loro differenziazione in neuroni con un fenotipo DA ha permesso la valutazione diretta dei meccanismi cellulari del PD e del Parkinsonismo, il meccanismo d'azione dei farmaci antiparkinsoniani e le applicazioni esplorative di vari aspetti della terapia cellulare. Lo scopo di questa tesi è la generazione e la caratterizzazione fenotipica di neuroni DA umani utilizzabili come strumento per lo sviluppo di una varietà di dispositivi terapeutici basati sulla terapia cellulare, in particolare dispositivi elettronici impiantabili interamente organici. Questi dispositivi sono stati progettati per essere impiantati in modelli animali di PD per una terapia loco-regionale guidata da stimoli elettrici e chimici per supportare l'attecchimento dei precursori dei neuroni DA, massimizzando la loro differenziazione e funzione. Al fine di ottenere precursori di neuroni DA umani di alta qualità e riproducibili che siano in grado di differenziarsi e maturare in neuroni DA funzionali che rispondono a stimoli elettrici e chimici, questo lavoro è stato organizzato in quattro sottoprogetti principali. Il primo sottoprogetto è stato dedicato all'ottimizzazione dei metodi di differenziazione delle iPSCs umane in precursori dei neuroni DA mesencefalici utilizzando un protocollo precedentemente pubblicato (Fedele et al. 2017). Questi precursori dei neuroni DA possono essere espansi per diversi passaggi e conservati in azoto liquido per qualsiasi uso futuro. Il secondo sottoprogetto è stato dedicato alla differenziazione dei precursori DA mesencefalici in neuroni DA maturi che sono stati caratterizzati mediante immunofluorescenza, PCR quantitativa, HPLC ed analisi elettrofisiologiche. Il fenotipo DA dei neuroni è stato studiato testando la loro risposta a due agonisti dopaminergici (pramipexolo e piribedil) attualmente utilizzati per il trattamento del PD. Dati recenti hanno dimostrato un effetto neurotrofico prodotto da un agonista antiparkinsoniano del recettore DA D2/D3, il ropinirolo (Collo et al. 2018). Sulla base di questi risultati, sono stati valutati gli effetti cellulari e molecolari di pramipexolo e piribedil sui neuroni DA umani studiando i cambiamenti morfologici correlati alla plasticità strutturale e l'attivazione delle vie intracellulari. Sono state studiate anche le proprietà neuroprotettive e neurorigenerative di questi due agenti farmacologici. Il terzo sottoprogetto è stato dedicato allo studio degli effetti della stimolazione elettrica sulla plasticità strutturale dei neuroni DA umani. Diversi lavori hanno dimostrato che la stimolazione elettrica può promuovere la differenziazione neuronale e la crescita dei neuriti di vari tipi di cellule neuronali in vitro, tra cui PC12 e cellule staminali neurali umane. Il quarto sottoprogetto è stato dedicato alla generazione di iPSCs umane da cellule mononucleate del sangue periferico (PBMCs) donate da nuovi controlli sani e pazienti affetti da un Parkinsonismo, l’atrofia multisistemica (MSA). I cloni di iPSCs ottenuti dal controllo e dal paziente sono stati sottoposti a caratterizzazione fenotipica per esaminare la presenza di marcatori di pluripotenza mediante immunofluorescenza, PCR quantitativa, analisi del cariotipo, pluripotenza e capacità di differenziazione nei tre foglietti embrionali. Le iPSCs sono state successivamente differenziate in neuroni DA mesencefalici e valutate per la loro risposta farmacologica agli agonisti dopaminergici.
The 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.
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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.

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La distonia DYT1 è una grave forma di distonia generalizzata causata da una mutazione del gene DYT1 che codifica per la proteina TorsinA. La funzione di tale proteina rimane ancora poco chiara anche se è stato proposto che possa svolgere importanti funzioni nel traffico proteico intracellulare e nei processi secretori. Lo striato, all'interno dei gangli della base svolge un importante ruolo nella regolazione dell'attività motoria, ed alterazioni a carico di tale struttura appaiono essere coinvolti nella patogenesi della distonia. Ho registrato pertanto le correnti sinaptiche spontanee sia di tipo GABAergico che glutamatergico in neuroni spinosi striatali (MSNs) da animali che sovraesprimevano la proteina umana mutata (hMT) confrontandoli poi con animali di controllo (CTRL) e con quelli che esprimevano la proteina umana non-mutata (hWT). Gli animali mutati presentavano un significativo aumento nella frequenza degli eventi sinaptici GABAergici (sIPSCs) non accompagnato però da variazioni nell'ampiezza di tali correnti. Al contrario l'attività spontanea di tipo glutamatergico (sEPSC) risultava essere del tutto normale. L'inibizione GABAergica striatale è di origine esclusivamente instrinseca e deriva da due distinte fonti. Una delle più importanti tuttavia fa capo agli interneuroni GABAergici Fast Spiking (FS). Ho pertanto verificato l'ipotesi che tali cellule potessero presentare alterazioni nella loro normale funzionalità. Sia gli sIPSCs che gli sEPSC registrati risultavano tuttavia essere invariati fra gli animali hMT, hWT e quelli di controllo. In condizioni fisiologiche l'attivazione del recettore dopaminergico D2 agisce presinapticamente inibendo il rilascio di GABA. Nei MSNs di animali di controllo e hWT, tale funzionalità risultava essere del tutto preservata. L'applicazione di quinpirolo (agonista D2-like) portava infatti ad una significativa riduzione della frequenza degli sIPSCs misurati. Tale effetto tuttavia era assente negli animali hMT. Inoltre sia MSNs sia FS di topi hMT non presentavano l'effetto inibitorio tipico del quinpirolo sulle correnti sinaptiche evocate tramite stimolazione elettrica (eIPSCs). In conclusione il mio lavoro dimostra la presenza di un'alterata attività del circuito GABAergico striatale in un modello animale di distonia DYT1, che può essere in parte giustificata da una disfunzione del recettore dopaminergico D2.
DYT1 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.
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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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Livres sur le sujet "Dopaminergici"

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Halász, B., K. Fuxe, L. F. Agnati, M. Kalia, M. Goldstein, K. Andersson, A. Härfstrand et B. Clark. The Dopaminergic System. Berlin, Heidelberg : Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69948-1.

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

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Umberto, Di Porzio, Pernas-Alonso Roberto et Perrone-Capano Carla, dir. Development of dopaminergic neurons. Austin : R.G. Landes Co., 1999.

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Woodruff, G. N., J. A. Poat et P. J. Roberts, dir. Dopaminergic Systems and their Regulation. London : Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0.

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N, Woodruff Geoffrey, Poat J. A, Roberts Peter J et International Congress of Pharmacology (9th : 1984 : London, England), dir. Dopaminergic systems and their regulation. Weinheim, Federal Republic of Germany : VCH Verlagsgesellschaft, 1986.

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N, Woodruff G., Poat J. A, Roberts P. J et IUPHAR International Congress of Pharmacology, (9th : 1984 : London), dir. Dopaminergic systems and their regulation. Basingstoke : Macmillan, 1986.

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Obeso, J. A., R. Horowski et C. D. Marsden, dir. Continuous Dopaminergic Stimulation in Parkinson’s Disease. Vienna : Springer Vienna, 1988. http://dx.doi.org/10.1007/978-3-7091-8954-2.

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Parkinson's disease : Role of continuous dopaminergic stimulation. Crowthorne : ESP Bioscience, 2012.

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Baron, J. C., D. Comar, L. Farde, J. L. Martinot et B. Mazoyer, dir. Brain Dopaminergic Systems : Imaging with Positron Tomography. Dordrecht : Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3528-3.

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Beart, P. M., G. N. Woodruff et D. M. Jackson, dir. Pharmacology and Functional Regulation of Dopaminergic Neurons. London : Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-10047-7.

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Chapitres de livres sur le sujet "Dopaminergici"

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Markstein, R., J. M. Vigouret, A. Enz, D. Coward, A. Jaton et U. Briner. « Dopaminergic Ergots ». Dans Pharmacology and Functional Regulation of Dopaminergic Neurons, 22–28. London : Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-10047-7_4.

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Seifert, Roland. « Dopaminergic System ». Dans Basic Knowledge of Pharmacology, 101–10. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18899-3_8.

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Halász, Béla. « Introduction to Neuroendocrinology ». Dans The Dopaminergic System, 1–9. Berlin, Heidelberg : Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69948-1_1.

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Fuxe, Kjell, Luigi F. Agnati, Madhu Kalia, Menek Goldstein, Kurt Andersson et Anders Härfstrand. « Dopaminergic Systems in the Brain and Pituitary ». Dans The Dopaminergic System, 11–25. Berlin, Heidelberg : Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69948-1_2.

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Clark, Barbara J. « The Role of Dopamine in the Periphery ». Dans The Dopaminergic System, 27–39. Berlin, Heidelberg : Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69948-1_3.

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Kuznetsov, Alexey, et Boris Gutkin. « Dopaminergic Cell Models ». Dans Encyclopedia of Computational Neuroscience, 1034–42. New York, NY : Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_86.

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McQuiston, Rory. « Mesolimbic Dopaminergic Projections ». Dans Encyclopedia of Clinical Neuropsychology, 2151. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_335.

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McQuiston, Rory. « Mesolimbic Dopaminergic Projections ». Dans Encyclopedia of Clinical Neuropsychology, 1. Cham : Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_335-2.

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Kuznetsov, Alexey, et Boris Gutkin. « Dopaminergic Cell Models ». Dans Encyclopedia of Computational Neuroscience, 1–11. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_86-2.

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McQuiston, Rory. « Mesolimbic Dopaminergic Projections ». Dans Encyclopedia of Clinical Neuropsychology, 1577. New York, NY : Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_335.

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Actes de conférences sur le sujet "Dopaminergici"

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Ordonez-Sanchez, Alejandro A., Omar Jimenez-Ramirez, Jose A. Cardenas-Valderrama, Mario Alan Quiroz-Juarez, Leonardo Palacios-Luengas et Ruben Vazquez Medina. « Generator of Synthetic Dopaminergic Signals ». Dans 2019 International Conference on Electronics, Communications and Computers (CONIELECOMP). IEEE, 2019. http://dx.doi.org/10.1109/conielecomp.2019.8673110.

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Comerford, James P., Steve Perryman, Amy Pruszenski, Frank Thorn et Richard Held. « Assessment of Lateral Interaction Across the Visual Field Using Hermann Grid Contrast Thresholds ». Dans Vision Science and its Applications. Washington, D.C. : Optica Publishing Group, 1997. http://dx.doi.org/10.1364/vsia.1997.sae.10.

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We have developed several psychophysical measures that may reflect the neuropharmacological control of center-surround interactions within the human visual system (Comerford et al 1990, 1991). We have been particularly interested in patients with Parkinson’s disease, a disease associated with destruction of the dopaminergic neurons of the Substantia Nigra (Comerford et al 1995). Recent evidence suggests that this disease also affects the dopaminergic neurons of the retina (Nguyen-Legros 1988). These retinal neurons release dopamine maximally under photopic conditions and are associated with an increase in surround inhibition in the center-surround balance of retinal receptive fields.
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Jaskir, Alana, et Michael Frank. « Computational advantages of dopaminergic states for decision making ». Dans 2019 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA : Cognitive Computational Neuroscience, 2019. http://dx.doi.org/10.32470/ccn.2019.1390-0.

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Liu, Ching-Lung, Chien-Fu F. Chen, Kuo-Hsing Ma et Yen-Ta Lu. « The effects of chronic intermittent hypoxia on dopaminergic neurodegeneration ». Dans ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2011.

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Mendes, Daniele Q., et Luis Alfredo V. de Carvalho. « Creativity and Delusions : The Dopaminergic Modulation of Cortical Maps ». Dans 5. Congresso Brasileiro de Redes Neurais. CNRN, 2016. http://dx.doi.org/10.21528/cbrn2001-072.

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Alavi, Azadeh, Brenton Cavanagh, Gervase Tuxworth, Adrian Meedeniya, Alan Mackay-Sim et Michael Blumenstein. « Automated classification of dopaminergic neurons in the rodent brain ». Dans 2009 International Joint Conference on Neural Networks (IJCNN 2009 - Atlanta). IEEE, 2009. http://dx.doi.org/10.1109/ijcnn.2009.5178740.

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Lavrova, Alina, Mikhail Akimov, Viktor Blokhin, Natalia Gretskaya et Vladimir Bezuglov. « NOVEL MULTIFUNCTIONAL COMPOUNDS FOR TARGETED DELIVERY TO DOPAMINERGIC NEURONS ». Dans XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1121.sudak.ns2020-16/291.

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Gonzalez-Lopez, Adrian, Alina Aguirre-Quevedo, Ines Lopez-Alonso, Estefania Batalla-Solis, Laura Amado-Rodriguez, Antonio Fueyo et Guillermo M. Albaiceta. « Mechanical Ventilation Triggers Hippocampal Apoptosis By Vagal And Dopaminergic Pahways ». Dans American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3068.

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Azuma, K., H. Takahashi, T. Kan, J. Tanimura, K. Ito, K. Matsumoto et I. Shimoyama. « Quantitative evaluation of the influence of dopaminergic neuron on flapping locomotion ». Dans 2013 IEEE 26th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2013. http://dx.doi.org/10.1109/memsys.2013.6474162.

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Dunovan, Kyle, Catalina Vich, Matthew Clapp, Jonathan Rubin et Timothy Verstynen. « Dopaminergic changes in striatal pathway competition modify specific cognitive decision parameters ». Dans 2018 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA : Cognitive Computational Neuroscience, 2018. http://dx.doi.org/10.32470/ccn.2018.1034-0.

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Rapports d'organisations sur le sujet "Dopaminergici"

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Przedborski, Serge. Role of Inflammation in MPTP-Induced Dopaminergic Degeneration. Fort Belvoir, VA : Defense Technical Information Center, décembre 2005. http://dx.doi.org/10.21236/ada446427.

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Przedborski, Serge, et Vernice Jackson-Lewis. Interaction of Synuclein and Inflammation in Dopaminergic Neurodegeneration. Fort Belvoir, VA : Defense Technical Information Center, juin 2014. http://dx.doi.org/10.21236/ada606023.

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Przedborski, Serge. Interaction of Synuclein and Inflammation in Dopaminergic Neurodegeneration. Fort Belvoir, VA : Defense Technical Information Center, juillet 2009. http://dx.doi.org/10.21236/ada506349.

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Przedborski, Serge. Interaction of Synuclein and Inflammation in Dopaminergic Neurodegeneration. Fort Belvoir, VA : Defense Technical Information Center, juillet 2010. http://dx.doi.org/10.21236/ada564265.

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Przedborski, Serge, et Vernice Jackson-Lewis. Interaction of Synuclein and Inflammation in Dopaminergic Neurodegeneration. Fort Belvoir, VA : Defense Technical Information Center, juillet 2012. http://dx.doi.org/10.21236/ada564270.

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Przedborski, Serge. Role of Inflammation in MPTP-Induced Dopaminergic Neuronal Death. Fort Belvoir, VA : Defense Technical Information Center, décembre 2008. http://dx.doi.org/10.21236/ada494929.

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Przedborski, Serge E. Role of Nitric Oxide in MPTP Induced Dopaminergic Neuron. Fort Belvoir, VA : Defense Technical Information Center, septembre 2000. http://dx.doi.org/10.21236/ada384796.

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Przedborski, Serge E. Role of Nitric Oxide in MPTP-Induced Dopaminergic Neuron Degeneration. Fort Belvoir, VA : Defense Technical Information Center, septembre 2004. http://dx.doi.org/10.21236/ada450371.

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Garris, Paul A., Tim Schallert et Byron A. Heidenreich. Phasic Dopaminergic Signaling and the Presymptomatic Phase of Parkinson's Disease. Fort Belvoir, VA : Defense Technical Information Center, juillet 2004. http://dx.doi.org/10.21236/ada430314.

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Przedborski, Serge. Role of Nitric Oxide in MPTP-Induced Dopaminergic Neuron Degeneration. Fort Belvoir, VA : Defense Technical Information Center, septembre 2002. http://dx.doi.org/10.21236/ada416386.

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