Relevant bibliographies by topics / Substanita nigra

Academic literature on the topic 'Substanita nigra'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Substanita nigra"

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Bannon, Michael J., and Christopher J. Whitty. "Neurokinin receptor gene expression in substantia nigra: localization, regulation, and potential physiological significance." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 866–70. http://dx.doi.org/10.1139/y95-119.

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Neurokinin receptor gene expression within the rat and human substantia nigra was examined in detail. In the rat, the relative abundances of nigral neurokinin receptor mRNAs were neurokinin 3 > neurokinin 1 [Formula: see text] neurokinin 2. High levels of neurokinin 3 mRNA were localized to dopamine neurons, as determined by dopamine cell lesions and colocalization with tyrosine hydroxylase mRNA. Stimulation of nigral neurokinin 3 receptors activated dopamine cells, as evidenced by increases in striatal dopamine metabolism and in a postsynaptic measure of dopamine neurotransmission (i.e., striatal substance P encoding mRNA). These and other anatomical and physiological data suggest that in the rat, substance P (released from striatonigral neurons) may act on nigral nondopamine cells through neurokinin 1 receptors, while the substance P cotransmitter neurokinin A may act preferentially on nigral dopamine neurons through neurokinin 3 receptors. Interestingly, high levels of neurokinin 1 (but not neurokinin 3) receptor mRNA are seen within human substantia nigra dopamine cells. Thus drugs interacting with neurokinin receptors may prove to be of value in the treatment of various neuropsychiatric disorders.Key words: neurokinin receptor, mRNA, dopamine, substantia nigra, human.
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Quijano, Aloia, Carmen Diaz-Ruiz, Andrea Lopez-Lopez, Begoña Villar-Cheda, Ana Muñoz, Ana I. Rodriguez-Perez, and Jose L. Labandeira-Garcia. "Angiotensin Type-1 Receptor Inhibition Reduces NLRP3 Inflammasome Upregulation Induced by Aging and Neurodegeneration in the Substantia Nigra of Male Rodents and Primary Mesencephalic Cultures." Antioxidants 11, no. 2 (February 8, 2022): 329. http://dx.doi.org/10.3390/antiox11020329.

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The tissue renin–angiotensin system (RAS) has been shown to be involved in prooxidative and proinflammatory changes observed in aging and aging-related diseases such as dopaminergic degeneration in Parkinson’s disease (PD). We studied the activation of the NLRP3 inflammasome in the substantia nigra with aging and early stages of dopaminergic degeneration in PD models and, particularly, if the brain RAS, via its prooxidative proinflammatory angiotensin II (AngII) type 1 (AT1) receptors, mediates the inflammasome activation. Nigras from aged rats and mice and 6-hydroxydopamine PD models showed upregulation in transcription of inflammasome-related components (NLRP3, pro-IL1β and pro-IL18) and IL1β and IL18 protein levels, which was inhibited by the AT1 receptor antagonist candesartan. The role of the AngII/AT1 axis in inflammasome activation was further confirmed in rats intraventricularly injected with AngII, and in primary mesencephalic cultures treated with 6-hydroxydopamine, which showed inflammasome activation that was blocked by candesartan. Observations in the nigra of young and aged AT1 and AT2 knockout mice confirmed the major role of AT1 receptors in nigral inflammasome activation. In conclusion, the inflammasome is upregulated by aging and dopaminergic degeneration in the substantia nigra, possibly related with a decrease in dopamine levels, and it is mediated by the AngII/AT1 axis.
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Wala, Elzbieta P., Jewell W. Sloan, and Xin Jing. "Substantia Nigra." Pharmacology Biochemistry and Behavior 64, no. 3 (November 1999): 611–23. http://dx.doi.org/10.1016/s0091-3057(99)00125-2.

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Garant, Douglas S., and Karen Gale. "Substantia nigra-mediated anticonvulsant actions: Role of nigral output pathways." Experimental Neurology 97, no. 1 (July 1987): 143–59. http://dx.doi.org/10.1016/0014-4886(87)90289-5.

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Biondetti, Emma, Rahul Gaurav, Lydia Yahia-Cherif, Graziella Mangone, Nadya Pyatigorskaya, Romain Valabrègue, Claire Ewenczyk, et al. "Spatiotemporal changes in substantia nigra neuromelanin content in Parkinson’s disease." Brain 143, no. 9 (August 28, 2020): 2757–70. http://dx.doi.org/10.1093/brain/awaa216.

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Abstract This study aimed to investigate the spatiotemporal changes in neuromelanin-sensitive MRI signal in the substantia nigra and their relation to clinical scores of disease severity in patients with early or progressing Parkinson’s disease and patients with idiopathic rapid eye movement sleep behaviour disorder (iRBD) exempt of Parkinsonian signs compared to healthy control subjects. Longitudinal T1-weighted anatomical and neuromelanin-sensitive MRI was performed in two cohorts, including patients with iRBD, patients with early or progressing Parkinson’s disease, and control subjects. Based on the aligned substantia nigra segmentations using a study-specific brain anatomical template, parametric maps of the probability of a voxel belonging to the substantia nigra were calculated for patients with various degrees of disease severity and controls. For each voxel in the substantia nigra, probability map of controls, correlations between signal-to-noise ratios on neuromelanin-sensitive MRI in patients with iRBD and Parkinson’s disease and clinical scores of motor disability, cognition and mood/behaviour were calculated. Our results showed that in patients, compared to the healthy control subjects, the volume of the substantia nigra was progressively reduced for increasing disease severity. The neuromelanin signal changes appeared to start in the posterolateral motor areas of the substantia nigra and then progressed to more medial areas of this region. The ratio between the volume of the substantia nigra in patients with Parkinson’s disease relative to the controls was best fitted by a mono-exponential decay. Based on this model, the pre-symptomatic phase of the disease started at 5.3 years before disease diagnosis, and 23.1% of the substantia nigra volume was lost at the time of diagnosis, which was in line with previous findings using post-mortem histology of the human substantia nigra and radiotracer studies of the human striatum. Voxel-wise patterns of correlation between neuromelanin-sensitive MRI signal-to-noise ratio and motor, cognitive and mood/behavioural clinical scores were localized in distinct regions of the substantia nigra. This localization reflected the functional organization of the nigrostriatal system observed in histological and electrophysiological studies in non-human primates (motor, cognitive and mood/behavioural domains). In conclusion, neuromelanin-sensitive MRI enabled us to assess voxel-wise modifications of substantia nigra’s morphology in vivo in humans, including healthy controls, patients with iRBD and patients with Parkinson’s disease, and identify their correlation with nigral function across all motor, cognitive and behavioural domains. This insight could help assess disease progression in drug trials of disease modification.
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Lersy, François, and Hamid Merdji. "Substantia Nigra Involvement." Neurology 97, no. 8 (May 26, 2021): 391–92. http://dx.doi.org/10.1212/wnl.0000000000012277.

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Toomsoo, Toomas, Inga Liepelt-Scarfone, Riina Kerner, Liis Kadastik-Eerme, Toomas Asser, Inna Rubanovits, Daniela Berg, and Pille Taba. "Substantia Nigra Hyperechogenicity." Journal of Ultrasound in Medicine 35, no. 1 (January 2016): 17–23. http://dx.doi.org/10.7863/ultra.14.12069.

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Tanibuchi, Ikuo, Hiroyuki Kitano, and Kohnosuke Jinnai. "Substantia Nigra Output to Prefrontal Cortex Via Thalamus in Monkeys. I. Electrophysiological Identification of Thalamic Relay Neurons." Journal of Neurophysiology 102, no. 5 (November 2009): 2933–45. http://dx.doi.org/10.1152/jn.91287.2008.

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A few studies have been performed in primate basal ganglia–thalamo–prefrontal pathways. Nevertheless, their electrophysiological properties and anatomical arrangements remain obscure. This study examined them in nigro-thalamo-cortical pathways from the substantia nigra pars reticulata (SNr) to the frontal cortex (FRC) via the mediodorsal (MD) and ventral anterior (VA) thalamus in monkeys. First, single thalamocortical neurons with SNr input were identified by antidromic responses to FRC stimulation and by inhibitory orthodromic responses with short latencies (<5 ms) to SNr stimulation. Second, single nigrothalamic neurons were found by antidromic responses to stimulation of the portions of the MD and VA where the thalamocortical neurons were recorded. The inhibitory orthodromic responses in the thalamocortical neurons were considered to be monosynaptically induced by nigral stimulation because the latency distribution of the orthodromic responses in the thalamocortical neurons was similar to that of the antidromic responses in the nigrothalamic neurons. Almost all relay neurons in the rostrolateral MD received inhibitory afferents from the caudolateral SNr and projected to the prefrontal area ventral to the principal sulcus, which constituted the densest nigro-thalamo-cortical projections. Meanwhile, neurons in the VA received inhibitory signals from the whole rostrocaudal extent of the SNr and projected to wide regions of the FRC; neurons in its pars magnocellularis mostly projected to different prefrontal areas, while those in its pars parvocellularis projected to motor areas. This report substantiated the topography of thalamocortical neurons monosynaptically receiving inhibitory SNr input and projecting to the FRC in the primate MD and VA at the single-neuron level.
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Simmons, DeNard V., Matthew H. Higgs, Sharmon Lebby, and Charles J. Wilson. "Indirect pathway control of firing rate and pattern in the substantia nigra pars reticulata." Journal of Neurophysiology 123, no. 2 (February 1, 2020): 800–814. http://dx.doi.org/10.1152/jn.00678.2019.

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Unitary pallido-nigral synaptic currents were measured using optogenetic stimulation, which activated up to three unitary synaptic inputs to each substantia nigra pars reticulata (SNr) cell. Episodic barrages of synaptic conductances were generated based on in vivo firing patterns of globus pallidus pars externa (GPe) cells and applied to SNr cells using conductance clamp. Barrage inputs were compared to continuous step conductances with the same mean. Barrage inputs and steps both slowed SNr neuron firing and produced disinhibition responses seen in peristimulus histograms. Barrages were less effective than steps at producing inhibition and disinhibition responses. Barrages, but not steps, produced irregular firing during the inhibitory response. Phase models of SNr neurons were constructed from their phase-resetting curves. The phase models reproduced the inhibition and disinhibition responses to the same inputs applied to the neurons. The disinhibition response did not require rebound currents but arose from reset of the cells’ oscillation. The differences in firing rate and irregularity in response to barrage and step inhibition resulted from the high sensitivity of SNr neurons to inhibition at late phases in their intrinsic oscillation. During step inhibition, cells continued rhythmic firing at a reduced rate. During barrages, brief bouts of intense inhibition stalled the cells’ phase evolution late in their cycle, close to firing, and even very brief respites from inhibition rapidly released single action potentials. The SNr cell firing pattern reflected the fine structure of the synaptic barrage from GPe, as well as its onset and offset. NEW & NOTEWORTHY The pallido-nigral pathway connects the striatum to spontaneously active basal ganglia output neurons in the substantia nigra. Each substantia nigra neuron receives powerful inhibitory synaptic connections from a small group of globus pallidus cells and may fire during pauses in pallidal activity. Despite lacking any hyperpolarization-activated rebound currents, they fire quickly to even brief pauses in the pallido-nigral inhibition. The mechanism of their rapid disinhibitory response is explained by features of their phase-resetting curves.
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Iribe, Yuji, Kevin Moore, Kevin C. H. Pang, and James M. Tepper. "Subthalamic Stimulation-Induced Synaptic Responses in Substantia Nigra Pars Compacta Dopaminergic Neurons In Vitro." Journal of Neurophysiology 82, no. 2 (August 1, 1999): 925–33. http://dx.doi.org/10.1152/jn.1999.82.2.925.

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The subthalamic nucleus (STN) is one of the principal sources of excitatory glutamatergic input to dopaminergic neurons of the substantia nigra, yet stimulation of the STN produces both excitatory and inhibitory effects on nigral dopaminergic neurons recorded extracellularly in vivo. The present experiments were designed to determine the sources of the excitatory and inhibitory effects. Synaptic potentials were recorded intracellularly from substantia nigra pars compacta dopaminergic neurons in parasagittal slices in response to stimulation of the STN. Synaptic potentials were analyzed for onset latency, amplitude, duration, and reversal potential in the presence and absence of GABA and glutamate receptor antagonists. STN-evoked depolarizing synaptic responses in dopaminergic neurons reversed at approximately −31 mV, intermediate between the expected reversal potential for an excitatory and an inhibitory postsynaptic potential (EPSP and IPSP). Blockade of GABAA receptors with bicuculline caused a positive shift in the reversal potential to near 0 mV, suggesting that STN stimulation evoked a near simultaneous EPSP and IPSP. Both synaptic responses were blocked by application of the glutamate receptor antagonist, 6-cyano-7-nitroquinoxalene-2,3-dione. The confounding influence of inhibitory fibers of passage from globus pallidus and/or striatum by STN stimulation was eliminated by unilaterally transecting striatonigral and pallidonigral fibers 3 days before recording. The reversal potential of STN-evoked synaptic responses in dopaminergic neurons in slices from transected animals was approximately −30 mV. Bath application of bicuculline shifted the reversal potential to ∼5 mV as it did in intact animals, suggesting that the source of the IPSP was within substantia nigra. These data indicate that electrical stimulation of the STN elicits a mixed EPSP-IPSP in nigral dopaminergic neurons due to the coactivation of an excitatory monosynaptic and an inhibitory polysynaptic connection between the STN and the dopaminergic neurons of substantia nigra pars compacta. The EPSP arises from a direct monosynaptic excitatory glutamatergic input from the STN. The IPSP arises polysynaptically, most likely through STN-evoked excitation of GABAergic neurons in substantia nigra pars reticulata, which produces feed-forward GABAA-mediated inhibition of dopaminergic neurons through inhibitory intranigral axon collaterals.
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Dissertations / Theses on the topic "Substanita nigra"

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Boyes, Justin. "The microcircuitry of the substantia nigra." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408818.

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Fan, Xiu-Di. "Substantia nigra dopamine infusion, behavioral and biochemical correlates." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32783.pdf.

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Häusser, Michael. "Intrinsic properties and synaptic inhibition of substantia nigra neurones." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306691.

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Richards, Christopher David. "Electrophysiology and electrochemistry of substantia nigra neurones in vitro." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259895.

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Barstow, Karen L. "Subthalamic control of dopamine release in the substantia nigra." Thesis, Boston University, 2001. https://hdl.handle.net/2144/36754.

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Thesis (Ph.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The overall goal of this dissertation was to determine the role of the subthalamic nucleus (STN) in regulating the release of dopamine in the substantia nigra (SN). Experiments first established the existence of a direct connection between subthalamic neurons and SN dopaminergic cells. Further experiments showed that this connection triggers the dopamine release in the SN, and the mechanisms involved in this release were determined. Whole-cell current clamp recordings were performed in parasagittal brain slices obtained from 10 to 16 day-old rat pups. Electrical stimulations of the STN reliably triggered excitatory post-synaptic potentials (EPSPs) in dopaminergic neurons of the SN pars compacta (SNc). Pharmacological experiments with specific receptor antagonists indicated that this EPSP was mediated by NMDA, non-NMDA and metabotropic glutamate receptors. Stimulations of the subthalamic input triggered the release of dopamine. In a subset of neurons in the SN pars reticulata (SNr), repetitive stimulations of the STN produced a summating EPSP that was followed by an inhibitory postsynaptic potential (IPSP). A D2 receptor antagonist blocked this IPSP suggesting that it represents the D2 receptor-mediated response of the recorded cell to dopamine released upon stimulation of the STN. Pharmacological experiments using this assay indicated that NMDA, non-NMDA or metabotropic glutamate receptors were individually not required for dendritic release of dopamine; however, each contributed to this release. In dopaminergic neurons located in the SN pars compacta, the inhibitory effect of dopamine was revealed following block of L-type Ca channels, NMDA and non-NMDA glutamate receptors. These results indicated that dopaminergic neurons located both in the SNc and SNr respond to the dendritic release of dopamine triggered upon stimulations of the STN. Finally, a specific blocker of the dopamine transporter (GBR12935) blocked the IPSP reversibly in both SNr and SNc dopaminergic neurons. If release occurred by exocytosis, block of the transporter should increase extracellular levels of dopamine and produce an increase in the size of the recorded IPSP. Therefore, these results suggest that dopamine dendritic release triggered by activation of the subthalamic input was mediated by reversed transport of dopamine rather than by exocytosis.
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McCormack, Alison. "The non-human primate as a model of human parkinsonism /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-624-7/.

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Last, A. T. J. "An electrophysiological study of neurochemical interactions in the substantia nigra." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382628.

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Threlfell, Sarah. "The histaminergic regulation of serotonin release in the substantia nigra." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432289.

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Hallett, James Matthew. "Evidence for GluN3-containing receptors in rat substantia nigra neurones." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607886.

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Fearnley, Julian Michael. "Regional substantia nigra selectivity in the pathology of movement disorders." Thesis, University College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319957.

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Books on the topic "Substanita nigra"

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Donkelaar, H. J. ten 1946-, ed. The human substantia nigra and ventral tegmental area: A neuroanatomical study with notes on aging and aging diseases. Berlin: Springer-Verlag, 1990.

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van Domburg, Peter Henricus Maria Franciscus, and Hendrik Jan ten Donkelaar. The Human Substantia Nigra and Ventral Tegmental Area. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75846-1.

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Giovanni, Giuseppe. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Vienna: Springer-Verlag Vienna, 2009.

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Giovanni, Giuseppe, Vincenzo Di Matteo, and Ennio Esposito, eds. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4.

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Rick, Caroline E. M. An electrophysiological study of substantia nigra pars reticlata neurones in vitro: Their regulation by gamma amino butyric acid and the actions of 5-hydroxytryptamine. Birmingham: University of Birmingham, 1995.

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Jon, Palfreman, ed. The case of the frozen addicts. New York: Pantheon Books, 1995.

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Illarioshkin, S. N., O. S. Levin, E. Y. Fedotova, and O. V. Kolokolov. Parkinsonism and the substantia nigra. Publishing Company «Аtmosphere, 2019. http://dx.doi.org/10.35165/978-5-902123-78-1.

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Peter Henricus M. F. Van Domburg, H. J. Ten Donkelaar, and P. H. M. F. Van Domburg. The Human Substantia Nigra and Ventral Tegmental Area: A Neuroanatomical Study With Notes on Aging and Aging Diseases (Advances in Anatomy, Embryology and Cell Biology). Springer, 1991.

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Esposito, Ennio, Vincenzo Di Matteo, and Giuseppe di Giovanni. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Springer, 2011.

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Esposito, Ennio, Vincenzo Di Matteo, and Giuseppe di Giovanni. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Springer, 2012.

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Book chapters on the topic "Substanita nigra"

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Leichnetz, George. "Substantia Nigra." In Encyclopedia of Clinical Neuropsychology, 3360–61. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_365.

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Leichnetz, George. "Substantia Nigra." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_365-2.

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Boie, Ioana. "Substantia Nigra." In Encyclopedia of Child Behavior and Development, 1457. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_2834.

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Bolling, Danielle. "Substantia Nigra." In Encyclopedia of Autism Spectrum Disorders, 3022. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_583.

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Bolling, Danielle. "Substantia Nigra." In Encyclopedia of Autism Spectrum Disorders, 4673–74. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_583.

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Leichnetz, George R. "Substantia Nigra." In Encyclopedia of Clinical Neuropsychology, 2433. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_365.

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Orme, R., RA Fricker-Gates, and MA Gates. "Ontogeny of Substantia Nigra Dopamine Neurons." In Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra, 3–18. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4_1.

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Arias-Carrión, Oscar, Elizabeth Yamada, Nils Freundlieb, Miriam Djufri, Lukas Maurer, Guido Hermanns, Bastian Ipach, et al. "Neurogenesis in Substantia Nigra of Parkinsonian Brains?" In Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra, 279–85. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4_23.

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Smidt, Marten P. "Specific Vulnerability of Substantia Nigra Compacta Neurons." In Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra, 39–47. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4_3.

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Guatteo, Ezia, Maria Letizia Cucchiaroni, and Nicola B. Mercuri. "Substantia Nigra Control of Basal Ganglia Nuclei." In Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra, 91–101. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4_7.

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Conference papers on the topic "Substanita nigra"

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Qureshi, Touseef Ahmad, Elliot Hogg, Lynch Cody, Debiao Li, Michele Tagliati, and Zhaoyang Fan. "Substantia nigra segmentation on neuromelanin-sensitive MRI." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor Gimi and Andrzej Krol. SPIE, 2019. http://dx.doi.org/10.1117/12.2512909.

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Basukala, Dibash, Ramakrishnan Mukundan, Tracy Melzer, and Ross Keenan. "Segmentation of Substantia Nigra Using Weighted Thresholding Method." In 2018 International Conference on Image and Vision Computing New Zealand (IVCNZ). IEEE, 2018. http://dx.doi.org/10.1109/ivcnz.2018.8634679.

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Trujillo, Paula, Alex K. Smith, Paul E. Summers, Luca M. Mainardi, Sergio Cerutti, Seth A. Smith, and Antonella Costa. "High-resolution quantitative imaging of the substantia nigra." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319619.

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Vezheeva, Olga, and Valeriy Sergeyev. "SUBNUCLEAR ORGANIZATION OF THE DOPAMINERGIC NEURONES IN THE RATS SUBSTANTIA NIGRA." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m979.sudak.ns2020-16/127-128.

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Basukala, Dibash, Ramakrishnan Mukundan, Tracy Melzer, and Ross Keenan. "Segmentation of Substantia Nigra for the Automated Characterization of Parkinson’s Disease." In 2018 IEEE International Conference on Image Processing, Applications and Systems (IPAS). IEEE, 2018. http://dx.doi.org/10.1109/ipas.2018.8708886.

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Rajendran, Arathi, Anuja Thankamani, Nishamol Nirmala, Bipin Nair, and Shyam Diwakar. "Computational neuroscience of substantia nigra circuit and dopamine modulation during parkinson's disease." In 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8125892.

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Salah, Zein, David Weise, Bernhard Preim, Joseph Classen, and Georg Rose. "Navigation-supported diagnosis of the substantia nigra by matching midbrain sonography and MRI." In SPIE Medical Imaging, edited by Bram van Ginneken and Carol L. Novak. SPIE, 2012. http://dx.doi.org/10.1117/12.911383.

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Basukala, Dibash, Ramakrishnan Mukundan, Tracy Melzer, and Anthony Lim. "Automated Segmentation of Substantia Nigra and Red Nucleus in Quantitative Susceptibility Mapping Images." In 2019 20th International Conference on Parallel and Distributed Computing, Applications and Technologies (PDCAT). IEEE, 2019. http://dx.doi.org/10.1109/pdcat46702.2019.00074.

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Hu, Tao, Hayato Itoh, Masahiro Oda, Shinji Saiki, Nobutaka Hattori, Koji Kamagata, Shigeki Aoki, and Kensaku Mori. "Size-reweighted cascaded fully convolutional network for substantia nigra segmentation from T2 MRI." In Image Processing, edited by Ivana Išgum and Olivier Colliot. SPIE, 2022. http://dx.doi.org/10.1117/12.2613298.

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10

McConnell, George C., and Warren M. Grill. "Stimulation location within the substantia nigra pars reticulata differentially modulates gait in hemiparkinsonian rats." In 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2013. http://dx.doi.org/10.1109/ner.2013.6696157.

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Reports on the topic "Substanita nigra"

1

Aronin, Neil. Protective Mechanisms Against Apoptic Neurodegeneration in the Substantia Nigra. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada415979.

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Aronin, Neil. Protective Mechanisms against Apoptic Neurodegeneration in the Substantia Nigra. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada390673.

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3

Surmeier, D. J. Calcium Homeostatasis and Mitochondrial Dysfunction in Dopaminergic Neurons of the Substantia Nigra. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada519458.

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Yanliang, Mei, Liu Xiaojing, Yuan Yanpeng, Li Lanjun, Xu Yuming, and Yang Jing. Transcranial sonography of substantia nigra for differential diagnosis of Parkinson's disease and other movement disorders: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0068.

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5

Andrades, Oscar, David Ulloa, Dario Martinez, Francisco Guede, Gustava Muñoz, Luis Javier Chirosa, and Amador García. Effect of the manipulation of the variables that configure the stimulus of strength training on motor symptoms in people with Parkinson's disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0079.

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Abstract:
Review question / Objective: To analyze the evidence on studies that have manipulated the variables that make up the strength training stimulus and its effects on motor symptoms in people with Parkinson's disease. Condition being studied: Parkinson's is a multisystemic neurodegenerative disease that affects the central nervous system and is caused by a loss of dopaminergic neurons in the compact part of the substantia nigra of the basal ganglia of the midbrain. People with Parkinson's disease (PEP) have non-motor and motor clinical symptoms. Classic motor symptoms are rest tremor, joint stiffness, bradykinesia, decreased balance, gait disturbances (speed, temporality, spatiality, support, and freezing) and decreased functional performance.
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Wang, Xiao, Hong Shen, Yujie Liang, Yixin Wang, Meiqi Zhang, and Hongtao Ma. Effectiveness of Tango Intervention on Motor Symptoms in Patients with Parkinson's Disease: A Protocol for Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0009.

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Review question / Objective: Parkinson's disease (PD) is a degenerative neurological disease caused by the loss of dopaminergic neurons in the pars compacta of the substantia nigra of the brain, resulting in lesions in the basal ganglia. The main motor symptoms of PD include resting tremor, rigidity, akinesia or bradykinesia and postural instability. As an exercise intervention based on musical accompaniment, tango dance has shown positive effects on the rehabilitation of motor symptoms in PD patients in recently. In this study, we systematically reviewed the efficacy of tango intervention in alleviating the motor symptoms of patients with PD. Condition being studied: Parkinson. Information sources: The following electronic databases will be searched: PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science Core collection, and China National Knowledge Infrastructure Database (CNKI) and WanFang Database.
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