Articles de revues : « Dopaminergici »

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Colao, Annamaria, et Renata Simona Auriemma. « Iperprolattinemia, farmaci dopaminergici e valvulopatie : vero o falso ? » L'Endocrinologo 13, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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, n^o 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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Orb, Sabine, Johannes Wieacker, Cesar Labarca, Carlos Fonck, Henry A. Lester et Johannes Schwarz. « Knockin mice with Leu9′Ser α4-nicotinic receptors : substantia nigra dopaminergic neurons are hypersensitive to agonist and lost postnatally ». Physiological Genomics 18, n^o 3 (11 août 2004) : 299–307. http://dx.doi.org/10.1152/physiolgenomics.00012.2004.

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This study analyzes the electrophysiological cause and behavioral consequence of dopaminergic cell loss in a knockin mouse strain bearing hypersensitive nicotinic α4-receptor subunits (“L9′S mice”). Adult brains of L9′S mice show moderate loss of substantia nigra dopaminergic neurons and of striatal dopaminergic innervation. Amphetamine-stimulated locomotion is impaired, reflecting a reduction of dopamine stored in presynaptic vesicles. Recordings from dopaminergic neurons in L9′S mice show that 10 μM nicotine depolarizes cells and increases spiking rates in L9′S cells but hyperpolarizes and decreases spiking rates in wild-type (WT) cells. Thus dopaminergic neurons of L9′S mice have an excitatory response to nicotine which is qualitatively different from that of WT neurons. The cause of dopaminergic cell death is therefore probably an increased sensitivity to acetylcholine or choline of α4-containing nicotinic receptors. Hypersensitive excitatory stimulation during activation of α4-containing receptors provides the first evidence for cholinergic excitotoxicity as a cause of dopaminergic neuron death. This novel concept may be relevant to the pathophysiology of Parkinson disease.

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Bohnen, Nicolaas. « Dopaminergic Vulnerability and Motor Impairments in Older Adults : Need for Targeted Pharmacotherapy ». Innovation in Aging 4, Supplement_1 (1 décembre 2020) : 757. http://dx.doi.org/10.1093/geroni/igaa057.2730.

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Abstract Motor impairments, including slow walking, are common in older age in the absence of prototypical Parkinson’s disease (PD). The etiology of such disturbances is heterogeneous and multi-system in nature. Dopamine is a key neurotransmitter involving motor, cognitive and behavioral circuitry. Normal aging is associated with substantial dopaminergic losses in the brain. Dopaminergic vulnerability of aging can be augmented by genotypic changes that may further compromise dopaminergic signaling, such as polymorphisms in the COMT gene. These observations may augur dopaminergic pharmacotherapy studies to treat gait disturbances in older adults. Prior dopaminergic therapy studies have shown overall limited effects in non-PD older adults. A major limitation of these studies is the non-targeted selection calling for personalized medicine approaches. Recent dopaminergic treatment studies targeting specific sub-groups of non-PD older adults conducted by us and others will be discussed.

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Obeso, J. A., J. Artieda et J. M. Martinez-Lage. « Dopaminergic photosensitivity ». Neurology 41, n^o 4 (1 avril 1991) : 612. http://dx.doi.org/10.1212/wnl.41.4.612-a.

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Palermo-Neto, João. « DOPAMINERGIC SYSTEMS ». Psychiatric Clinics of North America 20, n^o 4 (décembre 1997) : 705–21. http://dx.doi.org/10.1016/s0193-953x(05)70341-5.

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Chinta, Shankar J., et Julie K. Andersen. « Dopaminergic neurons ». International Journal of Biochemistry & ; Cell Biology 37, n^o 5 (mai 2005) : 942–46. http://dx.doi.org/10.1016/j.biocel.2004.09.009.

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Ryczko, Dimitri, Jackson J. Cone, Michael H. Alpert, Laurent Goetz, François Auclair, Catherine Dubé, Martin Parent, Mitchell F. Roitman, Simon Alford et Réjean Dubuc. « A descending dopamine pathway conserved from basal vertebrates to mammals ». Proceedings of the National Academy of Sciences 113, n^o 17 (11 avril 2016) : E2440—E2449. http://dx.doi.org/10.1073/pnas.1600684113.

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

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Hori, Yuria, Reiho Tsutsumi, Kento Nasu, Alex Boateng, Yasuhiko Ashikari, Masaharu Sugiura, Makoto Nakajima et al. « Aromatic-Turmerone Analogs Protect Dopaminergic Neurons in Midbrain Slice Cultures through Their Neuroprotective Activities ». Cells 10, n^o 5 (3 mai 2021) : 1090. http://dx.doi.org/10.3390/cells10051090.

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Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. The inflammatory activation of microglia participates in dopaminergic neurodegeneration in PD. Therefore, chemicals that inhibit microglial activation are considered to have therapeutic potential for PD. Aromatic (ar)-turmerone is a main component of turmeric oil extracted from Curcuma longa and has anti-inflammatory activity in cultured microglia. The aims of the present study are (1) to investigate whether naturally occurring S-enantiomer of ar-turmerone (S-Tur) protects dopaminergic neurons in midbrain slice cultures and (2) to examine ar-turmerone analogs that have higher activities than S-Tur in inhibiting microglial activation and protecting dopaminergic neurons. R-enantiomer (R-Tur) and two analogs showed slightly higher anti-inflammatory effects in microglial BV2 cells. S- and R-Tur and these two analogs reversed dopaminergic neurodegeneration triggered by microglial activation in midbrain slice cultures. Unexpectedly, this neuroprotection was independent of the inhibition of microglial activation. Additionally, two analogs more potently inhibited dopaminergic neurodegeneration triggered by a neurotoxin, 1-methyl-4-phenylpyridinium, than S-Tur. Taken together, we identified two ar-turmerone analogs that directly and potently protected dopaminergic neurons. An investigation using dopaminergic neuronal precursor cells suggested the possible involvement of nuclear factor erythroid 2-related factor 2 in this neuroprotection.

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Gaggi, Giulia, Andrea Di Credico, Pascal Izzicupo, Francesco Alviano, Michele Di Mauro, Angela Di Baldassarre et Barbara Ghinassi. « Human Mesenchymal Stromal Cells Unveil an Unexpected Differentiation Potential toward the Dopaminergic Neuronal Lineage ». International Journal of Molecular Sciences 21, n^o 18 (9 septembre 2020) : 6589. http://dx.doi.org/10.3390/ijms21186589.

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Degeneration of dopaminergic neurons represents the cause of many neurodegenerative diseases, with increasing incidence worldwide. The replacement of dead cells with new healthy ones may represent an appealing therapeutic approach to these pathologies, but currently, only pluripotent stem cells can generate dopaminergic neurons with high efficiency. However, with the use of these cells arises safety and/or ethical issues. Human mesenchymal stromal cells (hFM-MSCs) are perinatal stem cells that can be easily isolated from the amniochorionic membrane after delivery. Generally considered multipotent, their real differentiative potential is not completely elucidated. The aim of this study was to analyze their stemness characteristics and to evaluate whether they may overcome their mesenchymal fate, generating dopaminergic neurons. We demonstrated that hFM-MSCs expressed embryonal genes OCT4, NANOG, SOX2, KLF4, OVOL1, and ESG1, suggesting they have some features of pluripotency. Moreover, hFM-MSCs that underwent a dopaminergic differentiation protocol gradually increased the transcription of dopaminergic markers LMX1b, NURR1, PITX3, and DAT. We finally obtained a homogeneous population of cells resembling the morphology of primary midbrain dopaminergic neurons that expressed the functional dopaminergic markers TH, DAT, and Nurr1. In conclusion, our results suggested that hFM-MSCs retain the expression of pluripotency genes and are able to differentiate not only into mesodermal cells, but also into neuroectodermal dopaminergic neuron-like cells.

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Eyer, Gian-Carlo, Stefano Di Santo, Ekkehard Hewer, Lukas Andereggen, Stefanie Seiler et Hans Rudolf Widmer. « Co-Expression of Nogo-A in Dopaminergic Neurons of the Human Substantia Nigra Pars Compacta Is Reduced in Parkinson’s Disease ». Cells 10, n^o 12 (30 novembre 2021) : 3368. http://dx.doi.org/10.3390/cells10123368.

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Parkinson’s disease is mainly characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Together with the small number, the high vulnerability of the dopaminergic neurons is a major pathogenic culprit of Parkinson’s disease. Our previous findings of a higher survival of dopaminergic neurons in the substantia nigra co-expressing Nogo-A in an animal model of Parkinson’s disease suggested that Nogo-A may be associated with dopaminergic neurons resilience against Parkinson’s disease neurodegeneration. In the present study, we have addressed the expression of Nogo-A in the dopaminergic neurons in the substantia nigra in postmortem specimens of diseased and non-diseased subjects of different ages. For this purpose, in a collaborative effort we developed a tissue micro array (TMA) that allows for simultaneous staining of many samples in a single run. Interestingly, and in contrast to the observations gathered during normal aging and in the animal model of Parkinson’s disease, increasing age was significantly associated with a lower co-expression of Nogo-A in nigral dopaminergic neurons of patients with Parkinson’s disease. In sum, while Nogo-A expression in dopaminergic neurons is higher with increasing age, the opposite is the case in Parkinson’s disease. These observations suggest that Nogo-A might play a substantial role in the vulnerability of dopaminergic neurons in Parkinson’s disease.

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Shi, Weibo, Yaxing Zhang, Guoting Zhao, Songjun Wang, Guozhong Zhang, Chunling Ma, Bin Cong et Yingmin Li. « Dysregulation of Dopaminergic Regulatory Factors TH, Nurr1, and Pitx3 in the Ventral Tegmental Area Associated with Neuronal Injury Induced by Chronic Morphine Dependence ». International Journal of Molecular Sciences 20, n^o 2 (10 janvier 2019) : 250. http://dx.doi.org/10.3390/ijms20020250.

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The ventral tegmental area (VTA), a critical portion of the mesencephalic dopamine system, is thought to be involved in the development and maintenance of addiction. It has been proposed that the dopaminergic regulatory factors TH, Nurr1, and Pitx3 are crucial for determining the survival and maintenance of dopaminergic neurons. Thus, the present study investigated whether abnormalities in these dopaminergic regulatory factors in the VTA were associated with neuronal injury induced by chronic morphine dependence. Rat models with different durations of morphine dependence were established. Thionine staining was used to observe morphological changes in the VTA neurons. Immunohistochemistry and western blot were used to observe changes in the expression of the dopaminergic regulatory proteins TH, Nurr1, and Pitx3. Thionine staining revealed that prolonged morphine dependence resulted in dopaminergic neurons with edema, a lack of Nissl bodies, and pyknosis. Immunohistochemistry showed that the number of TH+, Nurr1+, and Pitx3+ cells, and the number of TH+ cells expressing Nurr1 or Pitx3, significantly decreased in the VTA after a long period of morphine dependence. Western blot results were consistent with the immunohistochemistry findings. Chronic morphine exposure resulted in abnormalities in dopaminergic regulatory factors and pathological changes in dopaminergic neurons in the VTA. These results suggest that dysregulation of dopaminergic regulatory factors in the VTA are associated with neuronal injury induced by chronic morphine dependence.

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Gray, Jeffrey A. « But the schizophrenia connection . . . » Behavioral and Brain Sciences 22, n^o 3 (juin 1999) : 523–24. http://dx.doi.org/10.1017/s0140525x99272044.

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As well as data indicating relationships (emphasised in the target article) (1) between dopaminergic transmission in the nucleus accumbens and positive incentive motivation, and (2) between dopaminergic transmission and extraversion, other data (not accounted for by the hypotheses developed in the target article) indicate relationships (3) between accumbens dopaminergic transmission and cognitive, especially perceptual, processes that are disrupted in schizophrenia, and (4) between dopaminergic transmission and psychoticism. The tension between relationships 1 + 2 and 3 + 4 is discussed and a tentative resolution proposed.

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Matera, Carlo, Pablo Calvé, Verònica Casadó-Anguera, Rosalba Sortino, Alexandre M. J. Gomila, Estefanía Moreno, Thomas Gener et al. « Reversible Photocontrol of Dopaminergic Transmission in Wild-Type Animals ». International Journal of Molecular Sciences 23, n^o 17 (4 septembre 2022) : 10114. http://dx.doi.org/10.3390/ijms231710114.

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Understanding the dopaminergic system is a priority in neurobiology and neuropharmacology. Dopamine receptors are involved in the modulation of fundamental physiological functions, and dysregulation of dopaminergic transmission is associated with major neurological disorders. However, the available tools to dissect the endogenous dopaminergic circuits have limited specificity, reversibility, resolution, or require genetic manipulation. Here, we introduce azodopa, a novel photoswitchable ligand that enables reversible spatiotemporal control of dopaminergic transmission. We demonstrate that azodopa activates D1-like receptors in vitro in a light-dependent manner. Moreover, it enables reversibly photocontrolling zebrafish motility on a timescale of seconds and allows separating the retinal component of dopaminergic neurotransmission. Azodopa increases the overall neural activity in the cortex of anesthetized mice and displays illumination-dependent activity in individual cells. Azodopa is the first photoswitchable dopamine agonist with demonstrated efficacy in wild-type animals and opens the way to remotely controlling dopaminergic neurotransmission for fundamental and therapeutic purposes.

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Baik, Ja-Hyun. « Stress and the dopaminergic reward system ». Experimental & ; Molecular Medicine 52, n^o 12 (décembre 2020) : 1879–90. http://dx.doi.org/10.1038/s12276-020-00532-4.

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AbstractDopamine regulates reward-related behavior through the mesolimbic dopaminergic pathway. Stress affects dopamine levels and dopaminergic neuronal activity in the mesolimbic dopamine system. Changes in mesolimbic dopaminergic neurotransmission are important for coping with stress, as they allow adaption to behavioral responses to various environmental stimuli. Upon stress exposure, modulation of the dopaminergic reward system is necessary for monitoring and selecting the optimal process for coping with stressful situations. Aversive stressful events may negatively regulate the dopaminergic reward system, perturbing reward sensitivity, which is closely associated with chronic stress-induced depression. The mesolimbic dopamine system is excited not only by reward but also by aversive stressful stimuli, which adds further intriguing complexity to the relationship between stress and the reward system. This review focuses on lines of evidence related to how stress, especially chronic stress, affects the mesolimbic dopamine system, and discusses the role of the dopaminergic reward system in chronic stress-induced depression.

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Dodson, Paul D., Jakob K. Dreyer, Katie A. Jennings, Emilie C. J. Syed, Richard Wade-Martins, Stephanie J. Cragg, J. Paul Bolam et Peter J. Magill. « Representation of spontaneous movement by dopaminergic neurons is cell-type selective and disrupted in parkinsonism ». Proceedings of the National Academy of Sciences 113, n^o 15 (21 mars 2016) : E2180—E2188. http://dx.doi.org/10.1073/pnas.1515941113.

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Midbrain dopaminergic neurons are essential for appropriate voluntary movement, as epitomized by the cardinal motor impairments arising in Parkinson’s disease. Understanding the basis of such motor control requires understanding how the firing of different types of dopaminergic neuron relates to movement and how this activity is deciphered in target structures such as the striatum. By recording and labeling individual neurons in behaving mice, we show that the representation of brief spontaneous movements in the firing of identified midbrain dopaminergic neurons is cell-type selective. Most dopaminergic neurons in the substantia nigra pars compacta (SNc), but not in ventral tegmental area or substantia nigra pars lateralis, consistently represented the onset of spontaneous movements with a pause in their firing. Computational modeling revealed that the movement-related firing of these dopaminergic neurons can manifest as rapid and robust fluctuations in striatal dopamine concentration and receptor activity. The exact nature of the movement-related signaling in the striatum depended on the type of dopaminergic neuron providing inputs, the striatal region innervated, and the type of dopamine receptor expressed by striatal neurons. Importantly, in aged mice harboring a genetic burden relevant for human Parkinson’s disease, the precise movement-related firing of SNc dopaminergic neurons and the resultant striatal dopamine signaling were lost. These data show that distinct dopaminergic cell types differentially encode spontaneous movement and elucidate how dysregulation of their firing in early Parkinsonism can impair their effector circuits.

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Machado, A., A. J. Herrera, J. L. Venero, M. Santiago, R. M. de Pablos, R. F. Villarán, A. M. Espinosa-Oliva et al. « Inflammatory Animal Model for Parkinson's Disease : The Intranigral Injection of LPS Induced the Inflammatory Process along with the Selective Degeneration of Nigrostriatal Dopaminergic Neurons ». ISRN Neurology 2011 (17 avril 2011) : 1–16. http://dx.doi.org/10.5402/2011/476158.

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We have developed an animal model of degeneration of the nigrostriatal dopaminergic neurons, the neuronal system involved in Parkinson's disease (PD). The implication of neuroinflammation on this disease was originally established in 1988, when the presence of activated microglia in the substantia nigra (SN) of parkinsonians was reported by McGeer et al. Neuroinflammation could be involved in the progression of the disease or even has more direct implications. We injected 2 μg of the potent proinflammatory compound lipopolysaccharide (LPS) in different areas of the CNS, finding that SN displayed the highest inflammatory response and that dopaminergic (body) neurons showed a special and specific sensitivity to this process with the induction of selective dopaminergic degeneration. Neurodegeneration is induced by inflammation since it is prevented by anti-inflammatory compounds. The special sensitivity of dopaminergic neurons seems to be related to the endogenous dopaminergic content, since it is overcome by dopamine depletion. Compounds that activate microglia or induce inflammation have similar effects to LPS. This model suggest that inflammation is an important component of the degeneration of the nigrostriatal dopaminergic system, probably also in PD. Anti-inflammatory treatments could be useful to prevent or slow down the rate of dopaminergic degeneration in this disease.

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Drobysheva, Daria, Kristen Ameel, Brandon Welch, Esther Ellison, Khan Chaichana, Bryan Hoang, Shilpy Sharma et al. « An Optimized Method for Histological Detection of Dopaminergic Neurons in Drosophila melanogaster ». Journal of Histochemistry & ; Cytochemistry 56, n^o 12 (2 septembre 2008) : 1049–63. http://dx.doi.org/10.1369/jhc.2008.951137.

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Parkinson's disease (PD) affects >1 million Americans and is marked by the loss of dopaminergic neurons in the substantia nigra. PD has been linked to two causative factors: genetic risks (hereditary PD) and environmental toxins (idiopathic PD). In recent years, considerable effort has been devoted to the development of a Drosophila model of human PD that might be useful for examining the cellular mechanisms of PD pathology by genetic screening. In 2000, Feany and Bender reported a Drosophila model of PD in which transgenic flies expressing human mutant α-synuclein exhibited shortened life spans, dopaminergic losses, Parkinsonian behaviors, and Lewy bodies in surviving dopaminergic neurons. Since then, a number of studies have been published that validate the model or build on it; conversely, a number report an inability to replicate the results and suggest that most protocols for dopaminergic histology underreport the actual numbers of dopaminergic neurons in the insect brain. Here we report the optimization of dopaminergic histology in Drosophila and identification of new dopaminergic neurons, show the remarkable dendritic complexity of these neurons, and provide an updated count of these neurons in adult brains. This manuscript contains online supplemental material at http://www.jhc.org . Please visit this article online to view these materials.

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Orcioli-Silva, Diego, Rodrigo Vitório, Priscila Nóbrega-Sousa, Victor Spiandor Beretta, Núbia Ribeiro da Conceição, Anderson Souza Oliveira, Marcelo Pinto Pereira et Lilian Teresa Bucken Gobbi. « Cortical Activity Underlying Gait Improvements Achieved With Dopaminergic Medication During Usual Walking and Obstacle Avoidance in Parkinson Disease ». Neurorehabilitation and Neural Repair 35, n^o 5 (23 mars 2021) : 406–18. http://dx.doi.org/10.1177/15459683211000736.

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Background Dopaminergic medication improves gait in people with Parkinson disease (PD). However, it remains unclear if dopaminergic medication modulates cortical activity while walking. Objective We investigated the effects of dopaminergic medication on cortical activity during unobstructed walking and obstacle avoidance in people with PD. Methods A total of 23 individuals with PD, in both off (PDOFF) and on (PDON) medication states, and 30 healthy older adults (control group [CG]) performed unobstructed walking and obstacle avoidance conditions. Cortical activity was acquired through a combined functional near-infrared spectroscopy electroencephalography (EEG) system, along with gait parameters, through an electronic carpet. Prefrontal cortex (PFC) oxygenated hemoglobin (HbO2) and EEG absolute power from FCz, Cz, and CPz channels were calculated. Results HbO2 concentration reduced for people with PDOFF during obstacle avoidance compared with unobstructed walking. In contrast, both people with PDON and the CG had increased HbO2 concentration when avoiding obstacles compared with unobstructed walking. Dopaminergic medication increased step length, step velocity, and β and γ power in the CPz channel, regardless of walking condition. Moreover, dopaminergic-related changes (ie, on-off) in FCz/CPz γ power were associated with dopaminergic-related changes in step length for both walking conditions. Conclusions PD compromises the activation of the PFC during obstacle avoidance, and dopaminergic medication facilitates its recruitment. In addition, PD medication increases sensorimotor integration during walking by increasing posterior parietal cortex (CPz) activity. Increased γ power in the CPz and FCz channels is correlated with step length improvements achieved with dopaminergic medication during unobstructed walking and obstacle avoidance in PD.

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Rangasamy, Suresh B., Sridevi Dasarathi, Aparna Nutakki, Shreya Mukherjee, Rohith Nellivalasa et Kalipada Pahan. « Stimulation of Dopamine Production by Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive ». Journal of Alzheimer's Disease Reports 5, n^o 1 (23 avril 2021) : 295–310. http://dx.doi.org/10.3233/adr-210001.

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Background: Parkinson’s disease (PD) is one of the most important neurodegenerative disorders in human in which recovery of functions could be achieved by improving the survival and function of residual dopaminergic neurons in the substantia nigra pars compacta. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in the dopamine (DA) biosynthesis pathway. Objective: Earlier our laboratory has shown that sodium benzoate (NaB), a metabolite of cinnamon and an FDA-approved drug against urea cycle disorders and glycine encephalopathy, increases neuroprotective molecules and protects dopaminergic neurons in a mouse model of PD. Here, we examined whether NaB could stimulate the production of DA in dopaminergic neurons. Methods: We employed PCR, real-time PCR, western blot, immunostaining, and HPLC to study the signature function of dopaminergic neurons. Locomotor functions were monitored in mice by open-field. Results: NaB increased the mRNA and protein expression of TH to produce DA in mouse MN9D dopaminergic neuronal cells. Accordingly, oral feeding of NaB increased the expression of TH in the nigra, upregulated striatal DA, and improved locomotor activities in striatum of normal C57/BL6 and aged A53T-α-syn transgenic mice. Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB. Conclusion: These results indicate a new function of NaB in which it may be beneficial in PD via stimulation of DA production from residual dopaminergic neurons.

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López-González del Rey, N., J. Blesa et J. A. Obeso. « Determinants of selective neuronal vulnerability in Parkinson's disease ». ANALES RANM 138, n^o 138(02) (31 août 2021) : 114–23. http://dx.doi.org/10.32440/ar.2021.138.02.rev01.

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Parkinson´s disease (PD) is the second most frequent neurodegenerative disease affecting the population older than 65 years old. This incidence will greatly increase due to the progressive aging of the population in the coming years. PD diagnosis is made when there is a 50-60% dopaminergic cell loss in the substantia nigra pars compacta (SNc) and the striatal dopamine loss reaches around 70-80%, coinciding with the onset of classical parkinsonian motor signs: tremor, rigidity and slowness of movement. A significant proportion of patients present non-motor symptoms, generally associated to disfunction of non-dopaminergic regions, which can appear before, around or after diagnosis (10-15 years). Therefore, in PD both dopaminergic and non-dopaminergic groups are affected, but the motor manifestations are the main reason for consultation and causes the greatest disability for many years. There is a large heterogeneity within dopaminergic neural groups in terms of morphology, metabolism, molecular pattern, protein accumulation, inflammation levels, protein expression, etc. In this review we discuss different factors that could explain the special vulnerability of certain dopaminergic neurons in the SNc. Knowledge on the mechanisms and underlying factors of this selective vulnerability of the ventrolateral dopaminergic neuros of the SNc is essential for developing neuromodulatory and/or neuroprotective therapies, leading in turn to halt or modify the neurodegenerative process in PD.

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Trenkwalder, C., J. Winkelmann et W. Paulus. « Dopaminergic and non-dopaminergic treatment in restless legs syndrome ». Journal of the Neurological Sciences 357 (octobre 2015) : e480. http://dx.doi.org/10.1016/j.jns.2015.09.231.

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Sakurada, K., M. Ohshima-Sakurada, T. D. Palmer et F. H. Gage. « Nurr1, an orphan nuclear receptor, is a transcriptional activator of endogenous tyrosine hydroxylase in neural progenitor cells derived from the adult brain ». Development 126, n^o 18 (15 septembre 1999) : 4017–26. http://dx.doi.org/10.1242/dev.126.18.4017.

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Adult rat-derived hippocampal progenitor cells express many of the molecules implicated in midbrain dopaminergic determination, including FGF receptors 1, 2 and 3, the sonic hedgehog receptor components Smo and Ptc, and the region-specific transcription factors Ptx3 and Nurr1. Here we use undifferentiated progenitors to probe the events leading to the dopaminergic phenotype and find that the influences of Nurr1 can be temporally and mechanistically uncoupled from the patterning influences of sonic hedgehog and FGF-8 or the more generic process of neuronal differentiation itself. In gain-of-function experiments, Nurr1 is able to activate transcription of the tyrosine hydroxylase gene by binding a response element within a region of the tyrosine hydroxylase promoter necessary for midbrain-specific expression. This activation is mediated through a retinoid X receptor independent mechanism and occurs in all precursors, regardless of differentiation status. Overexpression of Nurr1 does not affect proliferation or stimulate neuronal differentiation and has no influence on the expression of other dopaminergic markers. This uncoupling of tyrosine hydroxylase expression from other dopaminergic markers suggests that the midbrain dopaminergic identity is dictated by a combination of pan-dopaminergic (e.g., Shh/FGF-8) and region-specific (Nurr1) mechanisms.

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Rosenstein, Adam, Marcie Rabin et Roger Kurlan. « Augmentation in Restless Legs Syndrome : Treatment with Gradual Medication Modification ». Open Neurology Journal 9, n^o 1 (8 juin 2015) : 4–6. http://dx.doi.org/10.2174/1874205x01509010004.

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Dopaminergic drugs can cause augmentation during the treatment of restless legs syndrome (RLS). We previously reported that sudden withdrawal of dopaminergic treatment was poorly tolerated. We now report our experience with gradual withdrawal of the dopaminergic drug during the drug substitution process using a retrospective chart review with comparison to previous data. Seven patients with RLS and dopaminergic drug-induced augmentation were treated with a gradual withdrawal of the offending drug and replacement with an alternative medication. Compared to sudden withdrawal, measured outcomes were similar but gradual tapering was better tolerated. We conclude that for augmentation in RLS, gradual tapering of the augmentation-inducing dopaminergic drug is better tolerated than sudden withdrawal. The optimal approach to treating augmentation has not been established and may differ between patients. Further study with direct comparison of strategies and a larger patient population is needed to confirm our preliminary observations.

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Wei, Zhuang-Yao D., et Ashok K. Shetty. « Treating Parkinson’s disease by astrocyte reprogramming : Progress and challenges ». Science Advances 7, n^o 26 (juin 2021) : eabg3198. http://dx.doi.org/10.1126/sciadv.abg3198.

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Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder, is typified by both motor and nonmotor symptoms. The current medications provide symptomatic relief but do not stimulate the production of new dopaminergic neurons in the substantia nigra. Astrocyte reprogramming has recently received much attention as an avenue for increasing functional dopaminergic neurons in the mouse PD brain. By targeting a microRNA (miRNA) loop, astrocytes in the mouse brain could be reprogrammed into functional dopaminergic neurons. Such in vivo astrocyte reprogramming in the mouse model of PD has successfully added new dopaminergic neurons to the substantia nigra and increased dopamine levels associated with axonal projections into the striatum. This review deliberates the astrocyte reprogramming methods using specific transcription factors and mRNAs and the progress in generating dopaminergic neurons in vivo. In addition, the translational potential, challenges, and potential risks of astrocyte reprogramming for an enduring alleviation of parkinsonian symptoms are conferred.

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Matak, Pavle, Andrija Matak, Sarah Moustafa, Dipendra K. Aryal, Eric J. Benner, William Wetsel et Nancy C. Andrews. « Disrupted iron homeostasis causes dopaminergic neurodegeneration in mice ». Proceedings of the National Academy of Sciences 113, n^o 13 (29 février 2016) : 3428–35. http://dx.doi.org/10.1073/pnas.1519473113.

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Disrupted brain iron homeostasis is a common feature of neurodegenerative disease. To begin to understand how neuronal iron handling might be involved, we focused on dopaminergic neurons and asked how inactivation of transport proteins affected iron homeostasis in vivo in mice. Loss of the cellular iron exporter, ferroportin, had no apparent consequences. However, loss of transferrin receptor 1, involved in iron uptake, caused neuronal iron deficiency, age-progressive degeneration of a subset of dopaminergic neurons, and motor deficits. There was gradual depletion of dopaminergic projections in the striatum followed by death of dopaminergic neurons in the substantia nigra. Damaged mitochondria accumulated, and gene expression signatures indicated attempted axonal regeneration, a metabolic switch to glycolysis, oxidative stress, and the unfolded protein response. We demonstrate that loss of transferrin receptor 1, but not loss of ferroportin, can cause neurodegeneration in a subset of dopaminergic neurons in mice.

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Jauhar, S., M. Veronese, M. Rogdaki, M. Bloomfield, S. Natesan, F. Turkheimer, S. Kapur et O. D. Howes. « Regulation of dopaminergic function : an [18F]-DOPA PET apomorphine challenge study in humans. » Translational Psychiatry 7, n^o 2 (février 2017) : e1027-e1027. http://dx.doi.org/10.1038/tp.2016.270.

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Abstract Dopaminergic function has a key role in normal brain function, dopaminergic dysfunction being implicated in numerous neuropsychiatric disorders. Animal studies show that dopaminergic stimulation regulates dopaminergic function, but it is not known whether this exists in humans. In the first study (study 1), we measured dopamine synthesis capacity (indexed as K i cer) to identify the relationship between baseline and change in K i cer under resting conditions for comparison with effects of dopaminergic stimulation. In the second study (study 2), we used a within-subjects design to test effects of dopaminergic stimulation on dopamine synthesis capacity. In study 1, eight volunteers received two 18F-DOPA scans on separate days, both at rest. In study 2, 12 healthy male volunteers received two 18F-DOPA positron emission tomographic (PET) scans after treatment with either the dopamine partial agonist apomorphine (0.03 or 0.005 mg kg−1) or placebo. In study 1, no significant correlation was found between baseline and change in dopamine synthesis capacity between scans (r=−0.57, n=8, P=0.17, two-tailed). In study 2, a significant negative correlation was found between baseline dopamine synthesis capacity and percentage change in dopamine synthesis capacity after apomorphine challenge (r=−0.71, n=12, P=0.01, two-tailed). This correlation was significantly different (P<0.01) from the correlation between baseline and change in dopamine synthesis capacity under unstimulated conditions. One-way repeated-measures analysis of variance showed a significant group (study 1/study 2) × time interaction (F(1,18)=11.5, P=0.003). Our findings suggest that regulation of dopamine synthesis capacity by apomorphine depends on baseline dopamine function, consistent with dopamine stimulation stabilizing dopaminergic function. Loss of this autoregulation may contribute to dopaminergic dysfunction in brain disorders such as schizophrenia, substance dependence, and Parkinson's disease.

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

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Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease. Chronic pain is experienced by the vast majority of patients living with Parkinson’s disease. The degeneration of dopaminergic neuron acts as the essential mechanism of Parkinson’s disease in the midbrain dopaminergic pathway. The impairment of dopaminergic neurons leads to dysfunctions of the nociceptive system. Key cortical areas, such as the anterior cingulate cortex (ACC) and insular cortex (IC) that receive the dopaminergic projections are involved in pain transmission. Dopamine changes synaptic transmission via several pathway, for example the D2-adenly cyclase (AC)-cyclic AMP (cAMP)-protein kinase A (PKA) pathway and D1-G protein-coupled receptor kinase 2 (GRK2)-fragile X mental retardation protein (FMRP) pathway. The management of Parkinson’s disease-related pain implicates maintenance of stable level of dopaminergic drugs and analgesics, however a more selective drug targeting at key molecules in Parkinson’s disease-related pain remains to be investigated.

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Basile, Gianpaolo Antonio, Alessia Bramanti, Salvatore Bertino, Giuseppina Cutroneo, Antonio Bruno, Adriana Tisano, Giuseppe Paladina, Demetrio Milardi et Giuseppe Anastasi. « Structural Connectivity-Based Parcellation of the Dopaminergic Midbrain in Healthy Subjects and Schizophrenic Patients ». Medicina 56, n^o 12 (10 décembre 2020) : 686. http://dx.doi.org/10.3390/medicina56120686.

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Background and objectives: Functional deregulation of dopaminergic midbrain regions is a core feature of schizophrenia pathophysiology. Anatomical research on primates suggests that these regions may be subdivided into distinct, topographically organized functional territories according to their connectivity to the striatum. The aim of the present work was the reconstruction of dopaminergic midbrain subregions in healthy subjects and schizophrenic patients and the evaluation of their structural connectivity profiles. Materials and Methods: A hypothesis-driven connectivity-based parcellation derived from diffusion tractography was applied on 24 healthy subjects and 30 schizophrenic patients to identify distinct territories within the human dopaminergic midbrain in vivo and non-invasively. Results: We identified a tripartite subdivision of dopaminergic midbrain, including limbic, prefrontal and sensorimotor territories. No significant differences in structural features or connectivity were found between subjects and patients. Conclusions: The parcellation scheme proposed herein may help to achieve detailed characterization of structural and functional anomalies of the dopaminergic midbrain in schizophrenic patients.

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Rasheed, Naila, et Abdullah Alghasham. « Central Dopaminergic System and Its Implications in Stress-Mediated Neurological Disorders and Gastric Ulcers : Short Review ». Advances in Pharmacological Sciences 2012 (2012) : 1–11. http://dx.doi.org/10.1155/2012/182671.

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For decades, it has been suggested that dysfunction of dopaminergic pathways and their associated modulations in dopamine levels play a major role in the pathogenesis of neurological disorders. Dopaminergic system is involved in the stress response, and the neural mechanisms involved in stress are important for current research, but the recent and past data on the stress response by dopaminergic system have received little attention. Therefore, we have discussed these data on the stress response and propose a role for dopamine in coping with stress. In addition, we have also discussed gastric stress ulcers and their correlation with dopaminergic system. Furthermore, we have also highlighted some of the glucocorticoids and dopamine-mediated neurological disorders. Our literature survey suggests that dopaminergic system has received little attention in both clinical and preclinical research on stress, but the current research on this issue will surely identify a better understanding of stressful events and will give better ideas for further efficient antistress treatments.

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Lindvall, Olle. « Treatment of Parkinson's disease using cell transplantation ». Philosophical Transactions of the Royal Society B : Biological Sciences 370, n^o 1680 (19 octobre 2015) : 20140370. http://dx.doi.org/10.1098/rstb.2014.0370.

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The clinical trials with intrastriatal transplantation of human fetal mesencephalic tissue, rich in dopaminergic neurons, in Parkinson's disease (PD) patients show that cell replacement can work and in some cases induce major, long-lasting improvement. However, owing to poor tissue availability, this approach can only be applied in very few patients, and standardization is difficult, leading to wide variation in functional outcome. Stem cells and reprogrammed cells could potentially be used to produce dopaminergic neurons for transplantation. Importantly, dopaminergic neurons of the correct substantia nigra phenotype can now be generated from human embryonic stem cells in large numbers and standardized preparations, and will soon be ready for application in patients. Also, human induced pluripotent stem cell-derived dopaminergic neurons are being considered for clinical translation. Available data justify moving forward in a responsible way with these dopaminergic neurons, which should be tested, using optimal patient selection, cell preparation and transplantation procedures, in controlled clinical studies.

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Tomasella, Eugenia, Lucila Bechelli, Mora Belén Ogando, Camilo Mininni, Mariano N. Di Guilmi, Fernanda De Fino, Silvano Zanutto, Ana Belén Elgoyhen, Antonia Marin-Burgin et Diego M. Gelman. « Deletion of dopamine D2 receptors from parvalbumin interneurons in mouse causes schizophrenia-like phenotypes ». Proceedings of the National Academy of Sciences 115, n^o 13 (12 mars 2018) : 3476–81. http://dx.doi.org/10.1073/pnas.1719897115.

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Excessive dopamine neurotransmission underlies psychotic episodes as observed in patients with some types of bipolar disorder and schizophrenia. The dopaminergic hypothesis was postulated after the finding that antipsychotics were effective to halt increased dopamine tone. However, there is little evidence for dysfunction within the dopaminergic system itself. Alternatively, it has been proposed that excessive afferent activity onto ventral tegmental area dopaminergic neurons, particularly from the ventral hippocampus, increase dopamine neurotransmission, leading to psychosis. Here, we show that selective dopamine D2 receptor deletion from parvalbumin interneurons in mouse causes an impaired inhibitory activity in the ventral hippocampus and a dysregulated dopaminergic system. Conditional mutant animals show adult onset of schizophrenia-like behaviors and molecular, cellular, and physiological endophenotypes as previously described from postmortem brain studies of patients with schizophrenia. Our findings show that dopamine D2 receptor expression on parvalbumin interneurons is required to modulate and limit pyramidal neuron activity, which may prevent the dysregulation of the dopaminergic system.

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Jovanovic, Predrag, Yidan Wang, Jean-Philippe Vit, Edward Novinbakht, Nancy Morones, Elliot Hogg, Michele Tagliati et Celine E. Riera. « Sustained chemogenetic activation of locus coeruleus norepinephrine neurons promotes dopaminergic neuron survival in synucleinopathy ». PLOS ONE 17, n^o 3 (22 mars 2022) : e0263074. http://dx.doi.org/10.1371/journal.pone.0263074.

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Dopaminergic neuron degeneration in the midbrain plays a pivotal role in motor symptoms associated with Parkinson’s disease. However, non-motor symptoms of Parkinson’s disease and post-mortem histopathology confirm dysfunction in other brain areas, including the locus coeruleus and its associated neurotransmitter norepinephrine. Here, we investigate the role of central norepinephrine-producing neurons in Parkinson’s disease by chronically stimulating catecholaminergic neurons in the locus coeruleus using chemogenetic manipulation. We show that norepinephrine neurons send complex axonal projections to the dopaminergic neurons in the substantia nigra, confirming physical communication between these regions. Furthermore, we demonstrate that increased activity of norepinephrine neurons is protective against dopaminergic neuronal depletion in human α-syn A53T missense mutation over-expressing mice and prevents motor dysfunction in these mice. Remarkably, elevated norepinephrine neurons action fails to alleviate α-synuclein aggregation and microgliosis in the substantia nigra suggesting the presence of an alternate neuroprotective mechanism. The beneficial effects of high norepinephrine neuron activity might be attributed to the action of norepinephrine on dopaminergic neurons, as recombinant norepinephrine treatment increased primary dopaminergic neuron cultures survival and neurite sprouting. Collectively, our results suggest a neuroprotective mechanism where noradrenergic neurons activity preserves the integrity of dopaminergic neurons, which prevents synucleinopathy-dependent loss of these cells.

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Pignalosa, Francesca Chiara, Antonella Desiderio, Paola Mirra, Cecilia Nigro, Giuseppe Perruolo, Luca Ulianich, Pietro Formisano et al. « Diabetes and Cognitive Impairment : A Role for Glucotoxicity and Dopaminergic Dysfunction ». International Journal of Molecular Sciences 22, n^o 22 (16 novembre 2021) : 12366. http://dx.doi.org/10.3390/ijms222212366.

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Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia, responsible for the onset of several long-term complications. Recent evidence suggests that cognitive dysfunction represents an emerging complication of DM, but the underlying molecular mechanisms are still obscure. Dopamine (DA), a neurotransmitter essentially known for its relevance in the regulation of behavior and movement, modulates cognitive function, too. Interestingly, alterations of the dopaminergic system have been observed in DM. This review aims to offer a comprehensive overview of the most relevant experimental results assessing DA’s role in cognitive function, highlighting the presence of dopaminergic dysfunction in DM and supporting a role for glucotoxicity in DM-associated dopaminergic dysfunction and cognitive impairment. Several studies confirm a role for DA in cognition both in animal models and in humans. Similarly, significant alterations of the dopaminergic system have been observed in animal models of experimental diabetes and in diabetic patients, too. Evidence is accumulating that advanced glycation end products (AGEs) and their precursor methylglyoxal (MGO) are associated with cognitive impairment and alterations of the dopaminergic system. Further research is needed to clarify the molecular mechanisms linking DM-associated dopaminergic dysfunction and cognitive impairment and to assess the deleterious impact of glucotoxicity.

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Andersen, Anders H., Charles D. Smith, John T. Slevin, Richard J. Kryscio, Catherine A. Martin, Frederick A. Schmitt et Lee X. Blonder. « Dopaminergic Modulation of Medial Prefrontal Cortex Deactivation in Parkinson Depression ». Parkinson's Disease 2015 (2015) : 1–11. http://dx.doi.org/10.1155/2015/513452.

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Parkinson’s disease (PD) is associated with emotional abnormalities. Dopaminergic medications ameliorate Parkinsonian motor symptoms, but less is known regarding the impact of dopaminergic agents on affective processing, particularly in depressed PD (dPD) patients. The aim of this study was to examine the effects of dopaminergic pharmacotherapy on brain activation to emotional stimuli in depressed versus nondepressed Parkinson disease (ndPD) patients. Participants included 18 ndPD patients (11 men, 7 women) and 10 dPD patients (7 men, 3 women). Patients viewed photographs of emotional faces during functional MRI. Scans were performed while the patient was taking anti-Parkinson medication and the day after medication had been temporarily discontinued. Results indicate that dopaminergic medications have opposite effects in the prefrontal cortex depending upon depression status. DPD patients show greater deactivation in the ventromedial prefrontal cortex (VMPFC) on dopaminergic medications than off, while ndPD patients show greater deactivation in this region off drugs. The VMPFC is in the default-mode network (DMN). DMN activity is negatively correlated with activity in brain systems used for external visual attention. Thus dopaminergic medications may promote increased attention to external visual stimuli among dPD patients but impede normal suppression of DMN activity during external stimulation among ndPD patients.

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Fröhlich, Eleonore, Koroku Negishi et Hans-Joachim Wagner. « The occurrence of dopaminergic interplexiform cells correlates with the presence of cones in the retinae of fish ». Visual Neuroscience 12, n^o 2 (mars 1995) : 359–69. http://dx.doi.org/10.1017/s0952523800008038.

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AbstractUsing light-microscopic immunocytochemistry against tyrosine hydroxylase, we have investigated the morphology of dopaminergic cells in 23 species of fishes representing various systematic classes and subclasses and which live in very different habitats. We have, for the first time, observed teleosts with dopaminergic amacrine cells. Thus, in both bony and cartilaginous fishes, dopaminergic cells are differentiated as interplexiform and amacrine cells. The differentiation of dopaminergic cells into amacrine or interplexiform cells in fishes correlates with the absence or presence of cones. In pure-rod retinae, they occur as amacrine cells, and in mixed rod/cone retinae, they occur as interplexiform cells. We conclude therefore that the differentiation of retinal dopaminergic cells in fish does not depend on the evolutionary or systematic classification of a given species. Rather, it is correlated with the occurrence of rods and/or cones, and thus linked more closely to the habitat. We argue that, in fish, the presence of cones and cone-specific horizontal cells may be responsible for inducing dopaminergic cells to differentiate as interplexiform cells. Possible functions of dopamine in all-rod retinae, which may not require adaptation, may include neuromodulation in the inner plexiform layer for the sensitization of the rod pathway, the shaping of biological rhythms, and the control of eye growth.

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Li, Wen, Elisabet Englund, Håkan Widner, Bengt Mattsson, Danielle van Westen, Jimmy Lätt, Stig Rehncrona et al. « Extensive graft-derived dopaminergic innervation is maintained 24 years after transplantation in the degenerating parkinsonian brain ». Proceedings of the National Academy of Sciences 113, n^o 23 (2 mai 2016) : 6544–49. http://dx.doi.org/10.1073/pnas.1605245113.

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Clinical trials using cells derived from embryonic ventral mesencephalon have shown that transplanted dopaminergic neurons can survive and function in the long term, as demonstrated by in vivo brain imaging using 18F-fluorodopa and 11C-raclopride positron emission tomography. Here we report the postmortem analysis of a patient with Parkinson’s disease who 24 y earlier underwent unilateral transplantation of embryonic dopaminergic neurons in the putamen and subsequently exhibited major motor improvement and recovery of striatal dopaminergic function. Histopathological analysis showed that a dense, near-normal graft-derived dopaminergic reinnervation of the putamen can be maintained for a quarter of a century despite severe host brain pathology and with no evidence of immune response. In addition, ubiquitin- and α-synuclein–positive inclusions were seen, some with the appearance of typical Lewy bodies, in 11–12% of the grafted dopaminergic neurons, reflecting the spread of pathology from the host brain to the transplants. Because the clinical benefits induced by transplantation in this patient were gradually lost after 14 y posttransplantation, our findings provide the first reported evidence, to our knowledge, that even a viable dopaminergic graft giving rise to extensive striatal reinnervation may lose its efficacy if widespread degenerative changes develop in the host brain.

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Brooke-Jones, Megan, Martina Gáliková et Heinrich Dircksen. « Cyanobacterial Neurotoxin Beta-Methyl-Amino-l-Alanine Affects Dopaminergic Neurons in Optic Ganglia and Brain of Daphnia magna ». Toxins 10, n^o 12 (8 décembre 2018) : 527. http://dx.doi.org/10.3390/toxins10120527.

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The non-proteinogenic amino acid beta-methyl-amino-l-alanine (BMAA) is a neurotoxin produced by cyanobacteria. BMAA accumulation in the brain of animals via biomagnification along the food web can contribute to the development of neurodegenerative diseases such as Amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC), the latter being associated with a loss of dopaminergic neurons. Daphnia magna is an important microcrustacean zooplankton species that plays a key role in aquatic food webs, and BMAA-producing cyanobacteria often form part of their diet. Here, we tested the effects of BMAA on putative neurodegeneration of newly identified specific dopaminergic neurons in the optic ganglia/brain complex of D. magna using quantitative tyrosine-hydroxylase immunohistochemistry and fluorescence cytometry. The dopaminergic system was analysed in fed and starved isogenic D. magna adults incubated under different BMAA concentrations over 4 days. Increased BMAA concentration showed significant decrease in the stainability of dopaminergic neurons of D. magna, with fed animals showing a more extreme loss. Furthermore, higher BMAA concentrations tended to increase offspring mortality during incubation. These results are indicative of ingested BMAA causing neurodegeneration of dopaminergic neurons in D. magna and adversely affecting reproduction. This may imply similar effects of BMAA on known human neurodegenerative diseases involving dopaminergic neurons.

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Kao, Yu-Chia, Wei-Yen Wei, Kuen-Jer Tsai et Liang-Chao Wang. « High Fat Diet Suppresses Peroxisome Proliferator-Activated Receptors and Reduces Dopaminergic Neurons in the Substantia Nigra ». International Journal of Molecular Sciences 21, n^o 1 (27 décembre 2019) : 207. http://dx.doi.org/10.3390/ijms21010207.

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Although several epidemiologic and animal studies have revealed correlations between obesity and neurodegenerative disorders, such as Parkinson disease (PD), the underlying pathological mechanisms of obesity-induced PD remain unclear. Our study aimed to assess the effect of diet-induced obesity on the brain dopaminergic pathway. For five months, starting from weaning, we gave C57BL/6 mice a high-fat diet (HFD) to generate an obese mouse model and investigate whether the diet reprogrammed the midbrain dopaminergic system. Tyrosine hydroxylase staining showed that the HFD resulted in fewer dopaminergic neurons in the substantia nigra (SN), but not the striatum. It also induced neuroinflammation, with increased astrogliosis in the SN and striatum. Dendritic spine density in the SN of HFD-exposed mice decreased, which suggested that prolonged HFD altered dopaminergic neuroplasticity. All three peroxisome proliferator-activated receptor (PPAR) subtype (PPAR-α, PPAR-β/δ, PPAR-γ) levels were significantly reduced in the SN and the ventral tegmental area of HFD mice when compared to those in controls. This study showed that a prolonged HFD induced neuroinflammation, suppressed PPAR levels, caused degeneration of midbrain dopaminergic neurons, and resulted in symptoms reminiscent of human PD. To our knowledge, this is the first study documenting the effects of an HFD on PPARs in dopaminergic neurons.

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de Leeuw, Victoria C., Conny T. M. van Oostrom, Edwin P. Zwart, Harm J. Heusinkveld et Ellen V. S. Hessel. « Prolonged Differentiation of Neuron-Astrocyte Co-Cultures Results in Emergence of Dopaminergic Neurons ». International Journal of Molecular Sciences 24, n^o 4 (10 février 2023) : 3608. http://dx.doi.org/10.3390/ijms24043608.

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Dopamine is present in a subgroup of neurons that are vital for normal brain functioning. Disruption of the dopaminergic system, e.g., by chemical compounds, contributes to the development of Parkinson’s disease and potentially some neurodevelopmental disorders. Current test guidelines for chemical safety assessment do not include specific endpoints for dopamine disruption. Therefore, there is a need for the human-relevant assessment of (developmental) neurotoxicity related to dopamine disruption. The aim of this study was to determine the biological domain related to dopaminergic neurons of a human stem cell-based in vitro test, the human neural progenitor test (hNPT). Neural progenitor cells were differentiated in a neuron-astrocyte co-culture for 70 days, and dopamine-related gene and protein expression was investigated. Expression of genes specific for dopaminergic differentiation and functioning, such as LMX1B, NURR1, TH, SLC6A3, and KCNJ6, were increasing by day 14. From day 42, a network of neurons expressing the catecholamine marker TH and the dopaminergic markers VMAT2 and DAT was present. These results confirm stable gene and protein expression of dopaminergic markers in hNPT. Further characterization and chemical testing are needed to investigate if the model might be relevant in a testing strategy to test the neurotoxicity of the dopaminergic system.

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Nam, Min-Ho, Moonsun Sa, Yeon Ha Ju, Mingu Gordon Park et C. Justin Lee. « Revisiting the Role of Astrocytic MAOB in Parkinson’s Disease ». International Journal of Molecular Sciences 23, n^o 8 (18 avril 2022) : 4453. http://dx.doi.org/10.3390/ijms23084453.

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Monoamine oxidase-B (MAOB) has been believed to mediate the degradation of monoamine neurotransmitters such as dopamine. However, this traditional belief has been challenged by demonstrating that it is not MAOB but MAOA which mediates dopamine degradation. Instead, MAOB mediates the aberrant synthesis of GABA and hydrogen peroxide (H2O2) in reactive astrocytes of Parkinson’s disease (PD). Astrocytic GABA tonically suppresses the dopaminergic neuronal activity, whereas H2O2 aggravates astrocytic reactivity and dopaminergic neuronal death. Recently discovered reversible MAOB inhibitors reduce reactive astrogliosis and restore dopaminergic neuronal activity to alleviate PD symptoms in rodents. In this perspective, we redefine the role of MAOB for the aberrant suppression and deterioration of dopaminergic neurons through excessive GABA and H2O2 synthesis of reactive astrocytes in PD.

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Nutt, John G., et Nicolaas I. Bohnen. « Non-Dopaminergic Therapies ». Journal of Parkinson's Disease 8, s1 (18 décembre 2018) : S73—S78. http://dx.doi.org/10.3233/jpd-181472.

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