Дисертації з теми "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.
Повний текст джерелаFan, 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.
Повний текст джерелаHäusser, 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.
Повний текст джерелаRichards, 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.
Повний текст джерелаBarstow, Karen L. "Subthalamic control of dopamine release in the substantia nigra." Thesis, Boston University, 2001. https://hdl.handle.net/2144/36754.
Повний текст джерелаPLEASE 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.
2031-01-01
McCormack, Alison. "The non-human primate as a model of human parkinsonism /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-624-7/.
Повний текст джерелаLast, 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.
Повний текст джерелаThrelfell, 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.
Повний текст джерелаHallett, 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.
Повний текст джерелаFearnley, 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.
Повний текст джерелаBatista, Carla Isabel Soares. "Regulação dos níveis de GDNF na substantia nigra pelo estradiol." Master's thesis, Universidade de Aveiro, 2007. http://hdl.handle.net/10773/731.
Повний текст джерелаO stress oxidativo ao nível da via nigroestriatal é reconhecido como uma das causas da degeneração dos neurónios dopaminérgicos da substantia nigra na doença de Parkinson (DP), sendo o efeito protector do estradiol recorrentemente associado à protecção contra o stress oxidativo. A acção protectora do estradiol na via nigroestriatal pode ainda envolver outros efeitos, tais como modulação da expressão de factores neurotróficos cuja capacidade de promover a sobrevivência neuronal é sobejamente conhecida. Neste trabalho analisámos a regulação dos níveis do factor neurotrófico derivado de uma linha de células da glia (GDNF) pelo 17β-estradiol na substantia nigra e determinámos qual a contribuição específica deste efeito para a acção neuroprotectora da hormona. Adicionalmente, estudámos a modulação do efeito do 17β-estradiol na expressão de GDNF por agentes oxidantes, levodopa (L-DOPA) e H2O2. Para determinar os níveis de GDNF procedemos a análise de Western-Blot em extractos de células pós-natais de substantia nigra em cultura após incubação com 17ß-estradiol. Realizámos estudos in vivo para determinar de que forma o 17ß-estradiol afecta a acção da toxina dopaminérgica 6-hidroxidopamina (6-OHDA), quer ao nível da viabilidade das células dopaminérgicas, como ao nível da expressão dos níveis de GDNF. Os resultados obtidos permitiram concluir que, em células pós-natais de substantia nigra em cultura, o 17ß-estradiol promoveu o incremento da expressão do GDNF pelos astrócitos, provavelmente via ligação a receptores membranares. Verificámos ainda que os efeitos do estradiol parecem ser potenciados pela a exposição a L-DOPA e H2O2. In vivo, o estradiol protegeu as células dopaminérgicas da substantia nigra da lesão causada por 6-OHDA, possivelmente através da estimulação da síntese de GDNF observada nestas condições. ABSTRACT: Estradiol is currently considered a neuroprotector agent of nigral dopaminergic neurons. Oxidative stress in the nigrostriatal pathway has been associated with the development of Parkinson disease and the protective effect of estradiol is thought to be associated with a defence against oxidative stress. The protection promoted by estradiol in nigrostriatal pathway may also be coupled to the expression of neurotrophic factors, molecules recognized by its capability to promote neuron survival. In this study we analysed how 17ß-estradiol regulates nigral glial cell line deriv GDNF levels and evaluated the contribution of this effect to the neuroprotective action of this hormone. We also assessed how levodopa (L-DOPA) and H2O2 modulated the effect of estradiol on GDNF expression. Western-Blot analysis was used to determine GDNF levels in cultured substantia nigra cells after incubation with 17ß-estradiol. Using in vivo studies we evaluated how 17ß-estradiol affects the action of the dopaminergic toxin - 6- hidroxydopamine (6-OHDA) on the dopaminergic cell viability and the expression of GDNF. Taken together the results showed that, in cultured postnatal substantia nigra cells, 17ß-estradiol promoted the increase of GDNF expression by astrocytes through activation of putative membrane receptors. Exposure to the oxidative agents L-DOPA and H2O2 augmented the effect of estradiol. In vivo, estradiol protected nigral dopaminergic cells from 6-OHDA induced injury, possibly through stimulation of GDNF synthesis.
Hicks, Gareth A. "Adenosine 5'-triphosphate-sensitive potassium channels in the rat substantia nigra." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321402.
Повний текст джерелаO'Callaghan, John Francis Xavier. "Mechanisms in neurochemical modulation in the substantia nigra : an electrophysiological study." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260149.
Повний текст джерелаJohnson, Otto Luke Ross. "Physiological and anatomical control of burst firing in the substantia nigra." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268205.
Повний текст джерелаKapoor, Raju. "Studies of in vitro preparations of the cerebellum and substantia nigra." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.480555.
Повний текст джерелаYung, Wing Ho. "Physiology and morphology of substantia nigra pars compacta neurones in vitro." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280920.
Повний текст джерелаWild, Angela. "Regulation of NMDA receptors in substantia nigra pars compacta dopaminergic neurones." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608146.
Повний текст джерелаBrothwell, Shona Lindsay Crawford. "Properties of NMDA receptors in Substantia nigra pars compacta dopaminergic neurones." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612352.
Повний текст джерелаZhao, Q. "Activation properties and pharmacology of NMDA receptors in rat substantia nigra." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1386599/.
Повний текст джерелаWright, Kristina M. "Revising the Role of the Ventrolateral Periaqueductal Gray in the Fear Circuit:." Thesis, Boston College, 2021. http://hdl.handle.net/2345/bc-ir:109159.
Повний текст джерелаThesis advisor: John P. Christianson
The ability to accurately evaluate and respond to threats is vital to survival. Disruptions in neural circuits of fear give rise to maladaptive threat responding, and have clinical implications in fear and anxiety disorders. To better inform therapeutic interventions, it is imperative that roles for regions classically associated with fear continue to be refined, and that novel nodes are incorporated into what is most certainly a larger fear circuit. In the canonical view, threat estimates are generated at the level of the amygdala and sent to the ventrolateral periaqueductal gray (vlPAG), which organizes an appropriate behavioral response, most notably freezing. Despite a multitude of studies successfully linking the vlPAG and Pavlovian fear behavior, evidence of a direct neural correlate for fear expression in the vlPAG is lacking. By contrast, a role for the caudal substantia nigra (cSN) in fear, stands apart from its canonical associations with movement and reward processes. Although there is new interest in examining a role for the nigra in fear modulation, this is essentially an uncharted area of discovery. The goals of this dissertation are three-fold. First, to propose a role for vlPAG activity in threat estimation, a function previously restricted to the upstream amygdala. Second, to scrutinize vlPAG neural activity using a novel multi-cue Pavlovian procedure and identify the long-anticipated, direct neural correlate for fear expression. Third, to present causal evidence supporting the cSN as a potential node in a circuit that most certainly extends beyond regions canonically associated with fear
Thesis (PhD) — Boston College, 2021
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Psychology
葉天恒 and Tin-hang James Yip. "Emotion recognition in patients with Parkinson's disease: contribution of the substantia nigra." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31227016.
Повний текст джерелаKingsbury, Ann Elizabeth. "In situ hybridization studies of human substantia nigra : pathophysiology of Parkinson's disease." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398427.
Повний текст джерелаYip, Tin-hang James. "Emotion recognition in patients with Parkinson's disease : contribution of the substantia nigra /." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B24873007.
Повний текст джерелаFeddersen, Berend. "Contrôle des crises épileptiques par les ganglions de la base : approches expérimentale et clinique." Grenoble 1, 2009. http://www.theses.fr/2009GRE10111.
Повний текст джерелаAs about one third of epileptic patients are resistant to antiepileptic drugs, and only 30% of them are candidates for resective surgery, it exists a great demand for the development of alternative surgical therapies. It has been shown in animal studies, that the basal ganglia and especially the substantia nigra (SN) are involved in the control of epilepsy. Clinical evidence, using either electrophysiological or imaging approaches, also supports the involvement of the basal ganglia in some epileptic syndromes. The influence of seizure spread into the basal ganglia in patients with focal epilepsies was investigated on the rate of secondary generalization. We showed that activation of the basal ganglia was associated with an inhibitory effect on seizure propagation, when seizures spread into the frontal lobe. The elucidation of inhibitory mechanisms in epilepsy may open a new approach for therapeutic strategies such as electrical deep brain stimulation. First open case series, investigating deep brain stimulation of the basal ganglia to suppress epileptic seizures, showed encouraging results in some patients. However, more preclinical studies are mandatory to investigate the optimal stimulation parameters. The aim of our experimental approach was to determine the optimal stimulation parameters to control spontaneous seizures in a genetic model of absence epilepsy in the rat. In this model, the optimal parameters of single substantia nigra pars reticulata (SNr) stimulation were determined as bilateral, bipolar, monophasic, 60 Hz frequency and 60 µs pulse width. When these parameters were used for repeated stimulations, no long-term suppression and even increase of the number of seizures was observed. A delay of at least 60 sec was necessary between stimulations to be fully effective. Although single high-frequency stimulation of the SNr can be used to suppress ongoing seizures, repeated stimulation are ineffective and could even aggravate seizures, thus supporting the need of closed-loop stimulation procedures to chronically suppress seizures in therapeutical applications. Such an adaptative device would be effective only when detectable changes heralds the seizure onset. In a genetic model of absence epilepsy such changes in the EEG-coherence between the left and right SNr could be identified. Such changes might be used as an hallmark for adaptative procedures like triggered single stimulation to avoid the occurrence of the presumed seizures. To date it remains unknown, if such changes in coherence between left and right SNr, are specific to the model of GAERS and if such changes occur also in other animal models or humans with different epileptic syndromes. Accumulating evidences support that epilepsy is not a pathology restricted to the cortex as a seizure generator, but that subcortical structures are also involved, which might open new therapeutic options for patients who are pharmacoresistant and no candidates for a resective surgical treatment
Brown, Matthew Thomas Clifford. "Electrophysiological Neurochemical and morphological characterisation of the dopaminergic neurons in the substantia Nigra." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504319.
Повний текст джерелаFathinia, Panteha [Verfasser]. "Die Bedeutung der Hyperechogenität der Substantia nigra bei der Amyotrophen Lateralsklerose / Panteha Fathinia." Ulm : Universität Ulm, 2018. http://d-nb.info/1166757145/34.
Повний текст джерелаFarrant, M. "Inhibitory neurotransmission and amino acid release in the substantia nigra of the rat." Thesis, University College London (University of London), 1987. http://discovery.ucl.ac.uk/57623/.
Повний текст джерелаFalkenburger, Björn Henrik. "Freisetzung von Dopamin aus Dendriten dopaminerger Neurone der Substantia nigra durch den Dopamin-Transporter." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965704343.
Повний текст джерелаDuke, Dawn. "Expression profiling of the parkinsonian substantia nigra : towards a molecular defination of regional vulnerability." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497503.
Повний текст джерелаKimm, Tilia. "Potassium and Sodium Currents Regulating Pacemaking and Burst Firing in Substantia Nigra Dopamine Neurons." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226104.
Повний текст джерелаKeegan, Karl David. "Analysis of neurotensin and tachykinin receptor-mediated responses in the rat substantia nigra, in vitro." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282000.
Повний текст джерелаRöben, Benjamin [Verfasser], and Daniela [Akademischer Betreuer] Berg. "Hyperechogenität der Substantia nigra : Prävalenz und Assoziation mit kardiovaskulären Risikoprofilen / Benjamin Röben ; Betreuer: Daniela Berg." Tübingen : Universitätsbibliothek Tübingen, 2016. http://d-nb.info/1198120274/34.
Повний текст джерелаMorris, Paul George. "Functions of GluN2D-containing NMDA receptors in dopamine neurons of the substantia nigra pars compacta." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271850.
Повний текст джерелаTöllner, Kathrin. "Die Bedeutung der Substantia nigra pars reticulata für die Temporallappenepilepsie pharmakologische Manipulation und elektrophysiologische Messung." Giessen DVG-Service, 2009. http://library.vetmed.fu-berlin.de/ResourceList/details/202703.
Повний текст джерелаCARDOSO, Henriqueta Dias. "Mecanismos neuroquímicos envolvidos na neurodegeneração da Substantia nigra pela restrição dietética em ácidos graxos essenciais." Universidade Federal de Pernambuco, 2013. https://repositorio.ufpe.br/handle/123456789/13273.
Повний текст джерелаMade available in DSpace on 2015-04-17T12:44:08Z (GMT). No. of bitstreams: 2 Tese Henriqueta Dias Cardoso.pdf: 5265290 bytes, checksum: e2e8c3ba450de08f6e92ede26a203fc0 (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Previous issue date: 2013-02-26
FACEPE
Os ácidos graxos essenciais (AGEs) têm sido indicados como potenciais agentes preventivos e terapêuticos em uma grande variedade de doenças neurodegenerativas assim como indispensáveis para o desenvolvimento cerebral. O principal objetivo deste trabalho foi investigar os mecanismos relacionados com a perda de neurônios dopaminérgicos induzida pela deficiência crônica em AGEs previamente detectada na substância negra (SN) de ratos Wistar jovens (J), estendendo a análise também a animais adultos (A). Para isso, foram utilizadas dietas balanceadas e que diferiram apenas na fonte lipídica, sendo óleo de soja para os grupos controles (C) e óleo de coco para os grupos experimentais (E). As dietas foram fornecidas às mães a partir do acasalamento e mantidas por uma (F1) ou duas (F2) gerações. Marcadores de insulto oxidativo: lipoperoxidação (LP), atividade das enzimas superóxido dismutase total (SOD-t), catalase (CAT) na SN e corpo estriado (CE) foram avaliados em animais AF1 e em JF2 e AF2. Indicadores de neurodegeneração na SN e CE destes animais foram avaliados utilizando a técnica de marcação com o fluoróforo, Fluoro Jade C. Análise quantitativa do tamanho e nº de neurônios dopaminérgicos e da distribuição de células imunorreativas ao fator neurotrófico derivado do cérebro (BDNF) foi realizada em animais AF2. Os níveis de nitrito, como indicador da produção de óxido nítrico na SN e CE, foram analisados em animais JF2 e AF2. A dieta experimental reduziu em ~28%, ~50% e ~60% os níveis de ácido docosahexaenóico (DHA) na SN dos grupos experimentais AF1, JF2 e AF2 respectivamente, comparado aos seus controles. Nos animais EAF1 um aumento em ~17% e ~45% na atividade da SOD-t foi observado na SN e CE comparado ao grupo controle, o evitou níveis danosos de lipoperoxidação. Por outro lado, um aumento nos níveis de lipoperoxidação (~34%) foi detectado na SN de animais EJF2, acompanhados de não reatividade da SOD-t e de uma redução em 4,8 vezes na atividade da CAT. Sinais de neurodegeneração foram evidenciados em neurônios dopaminérgicos e não dopaminérgicos da SN do grupo EJF2. No CE, o aumento da LP em ~39% foi acompanhado de redução em 3,8 vezes e 2,8 vezes da atividade da SOD-t e CAT, respectivamente, só foram observados nos animais do grupo EAF2. A dieta experimental não alterou os níveis de nitrito na SN, mas aumentou de forma significativa estes níveis no CE de animais jovens (30%) e adultos (1,8 vezes). A deficiência crônica em DHA até a idade adulta comprometeu o crescimento do corpo celular e aumentou a perda de neurônios dopaminérgicas na SN rostro-dorso-medial (~35%) afetando também aqueles localizados na região caudo-ventro-lateral deste núcleo. Uma redução de ~22% no número de células BDNF+ foi também observada na SN. Os resultados mostram que a restrição dietética em AGEs por duas gerações até a idade adulta é capaz de induzir lipoperoxidação na SN e CE devido a comprometimento na atividade das enzimas anti-oxidantes, perda de células BDNF+ na SN e aumentados níveis de óxido nítrico no CE. Tidos em conjunto, tais mecanismos podem estar atuando de forma sinérgica na degeneração de neurônios dopaminérgicos induzida pela deficiência em DHA.
Ghorayeb, Imad. "Initiation d'analogues expérimentaux de la dégénérescence striatonigrique." Bordeaux 2, 2001. http://www.theses.fr/2001BOR28890.
Повний текст джерелаL-Dopa-unresponsive parkinsonism dominates the clinical syndrome of striatonigral degeneration (SND), a severe neurodegenerative disease which is caracterized by a dual pathology affecting nigral dopaminergic neurons and striatal output neurons. Experimental models reproducing salient pathological features are needed to better understand the underlying pathophysiology of motor signs and dopa-unresponsiveness. We demonstrated the feasibility of such models in rodents as well as, and for the first time, in non-human primates. In rodents, a "double toxin-double lesion" using quinolinic acid (QA) + 6-OHDA and a "single toxin-double lesion" stereotaxic approache using MPP+ were explored, while in non-human primates systemic and sequential chronic MPTP + 3-nitropropionic acid (3NP) injections was used. In rodents, "specific" motor symptoms were induced by the combined striatal and nigral lesion that were different from those induced by a single striatal or nigral lesion. In primates, the most relevant clinical aspect is the subsequent occurence of a L-Dopa-responsive then of a L-Dopa-unresponsive parkinsonism. The latter was associated with a decreased density of dopaminoceptive medium spiny neurons of both the indirect and direct striatal outflow pathways as observed in SND. Altogether, our results clearly demonstrate that basic SND clinical and pathological features can be reproduced in rodents as well as in non-human primates. These models will be helpful for exploring new therapeutics strategies (neuroprotection, neurorestoration, deep brain stimulation) prior to clinical applications
Bouyssières, Céline. "Induction de signaux calciques dans les cellules gliales de la substance noire réticulée par la stimulation électrique du noyau sous-thalamique." Grenoble 1, 2009. https://tel.archives-ouvertes.fr/tel-00414218.
Повний текст джерелаHigh-frequency stimulation of the subthalamic nucleus (STN-HFS) is an effective treatment for alleviating the motor symptoms of parkinsonian patients. However, the cellular and molecular mechanisms of its effects remain under debate. Marc Savasta's laboratory had previously shown that, in awake or anaesthetized rats, STN-HFS increased extracellular glutamate and GABA contents in one of the main output nuclei of the STN, substantia nigra pars reticulata (SNr). Within the SNr, data suggested that, under NST stimulation, the regulation of neuronal activity is conjointly due to the excitation of NST glutamatergic neurons and the involvement of GABAergic fibers coming from the GPe and passing near the stimulated area. The aim of the present study is to study glial cell implication in the cellular response to STN-HFS within the SNr, by using a calcium imaging technique in adult rat brain slices. Rat brain horizontal slices, containing both STN and SNr, and respecting at best their glutamatergic connections, were used. We show by immunochemistry that the SNr contains 32% of neuron versus 68% of glial cells. Then, we show that STN-HFS induced a calcium response in almost 12% of SNr glial cells population. These calcium responses involved the release of glutamate, GABA and ATP within the SNr. Thus, this study shows that glutamate and GABA, known to be released within SNr under STN-HFS, are able to activate glial cells. Moreover, it provides evidence that ATP, one of the main gliotransmitter, is released within the SNr under STN-HFS. Thus, SNr glial cells respond to the STN-HSF and could potentially be involved in the modulation of neuronal activity in this structure
Kanter, Marlene. "Organisationsprinzipien der extrazellulären Matrix in der Substantia nigra des Menschen und ihr Bezug zum Morbus Parkinson." Doctoral thesis, Universitätsbibliothek Leipzig, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-62572.
Повний текст джерелаPfreundtner, Claudia. "Wirkung von Cannabinoiden auf die Neurotransmission im Corpus striatum und in der Substantia nigra pars reticulata." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972359540.
Повний текст джерелаSchaeff, Sulamith [Verfasser], Marcel [Gutachter] Romanos, and Camelia-Maria [Gutachter] Monoranu. "Correlates of Substantia Nigra Echogenicity in Healthy Children / Sulamith Schaeff ; Gutachter: Marcel Romanos, Camelia-Maria Monoranu." Würzburg : Universität Würzburg, 2021. http://d-nb.info/1229352503/34.
Повний текст джерелаHetzer, Anna Maria [Verfasser]. "Die exofokale postischämische neuronale Degeneration der Substantia nigra nach striatalem Infarkt im Mausmodell / Anna Maria Hetzer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1076038697/34.
Повний текст джерелаDelgado, Zabalza Lorena. "Electrophysiological characterization of neuronal diversity in the substantia nigra pars reticulata in control and parkinsonian mice." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0052.
Повний текст джерелаThe substantia nigra pars reticulate (SNr) is the main output structure of the basal ganglia (BG), a subcortical network controlling the elaboration of motor programs as well as cognitive and associative learning functions. The identification of distinct cell-types within the BG has played a key role for understanding the properties and functions of this circuit. Recent studies suggest that the SNr is composed of several cell types but until now this neuronal diversity has never been taken into consideration regarding normal and pathological functioning of this nucleus, particularly in Parkinson’s disease (PD). By combining immunohistochemical and electrophysiological approaches in the PVCre::Ai9T mouse line, we have demonstrated that SNr neurons expressing the protein parvalbumin (PV+) exhibit different anatomical and electrophysiological properties than non PV-expressing (PV-) neurons. Our anatomical analysis reveal that PV+ and PV- neurons are present in equal proportion in the SNr, but with a distinct distribution, PV+ being enriched in the lateral part of the SNr, while PV- are found in the medial portion of the nucleus. In vitro electrophysiological recordings from identified PV+ and PV- neurons in the SNr also revealed that PV+ neurons fired at relatively higher rates than PV- cells. Additionally, our data revealed that DA loss and subsequent L-DOPA treatment induce a profound reduction of the excitability of PV+ SNr neurons in a 6-OHDA mouse model of PD while activity of PV- remains unchanged by these treatments.It is well known that the activity of SNr neurons is controlled by GABAergic inputs from striatal dSPN and the GP. We performed optogenetic manipulation of STR-SNr and GP-SNr inputs in order to determine whether PV+ and PV- SNr neurons received equivalent inputs from these two nuclei. We tested the impact of STR-SNr or GP-SNr activation on the activity of SNr neurons in cell-attached configuration and then switched to whole-cell voltage-clamp to characterize short-term plasticity of these synapses. Our results show that both PV+ and PV- SNr neurons are innervated by the STR and the GP. They also revealed that inhibition from dSPN was more powerful to silence activity of both subtypes of SNr neurons. Indeed, we observed that both STR-SNr and GP-SNr synapses displayed short-term depression in PV+ and PV- SNr neurons. DA loss affected GABA transmission in a different manner in PV+ and PV- SNr cells. On one hand, PV+ neurons were more sensible to striatal synaptic inhibition than PV- cells after DA depletion. On the other hand, PV-GP inputs were reduced on PV+ neurons and increased in PV- cells after DA loss suggesting a disequilibrium in pallidal inhibition between these two SNr populations.Furthermore, considering that rodent models of PD have shown elevated extracellular levels of GABA in the SNr which can exert a tonic extrasynaptic inhibition on SNr neurons, we decided to characterize GABAergic extrasynaptic transmission in the SNr of control and 6-OHDA lesioned mice. We studied GABAA mediated tonic inhibition by performing whole-cell patch-clamp recordings of PV+ and PV- SNr neurons in acute slices. We observed that PV- SNr neurons displayed larger GABAA receptor-mediated tonic currents than PV+ cells in the SNr of control mice. The presence and involvement of δ and/or α5 extrasynaptic subunits in GABAA receptors mediating this type of transmission was also studied, revealing a major presence and effect of α5-subunits on PV- neurons probably mediating the tonic currents observed in these neurons. However, contrary to expected, chronic DA-depletion did not trigger any increase in tonic inhibition neither in PV+ cells nor in PV- SNr neurons.All these findings highlight the importance of differentiating cell populations in the SNr to a better knowledge of the BG circuit in normal and pathological states such as in PD
Heiland, Bettina. "Die nicht-cholinerge Funktion der Azetylcholinesterase in dopaminergen Gebieten des ZNS in gesunden, pathologischen und sich entwickelnden Systemen The non-cholinergic function of acetylcholinesterase in the dopaminergic areas of the CNS in healthy, pathological and developing systems /." [S.l.] : [s.n.], 2002. http://elib.tu-darmstadt.de/diss/000319.
Повний текст джерелаChen, Yan. "EFFECTS OF GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTOR (GDNF) ON STEM/PROGENITOR CELL PROLIFERATION AND DIFFERENTIATION." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/233.
Повний текст джерелаAkaoka, Hidéo. "Régulation dopaminergique de l'activité électrique des neurones du système nigro-strié." Lyon 1, 1990. http://www.theses.fr/1990LYO1T008.
Повний текст джерелаRheey, Jinguen. "Otx2 promotes survival of injured adult retinal ganglion cells non cell-autonomously and regulates development of inner retinal cells in post-natal mouse cell autonomously." Paris 6, 2011. http://www.theses.fr/2011PA066176.
Повний текст джерелаDickerson, Jonathan W. "Neuroprotective and neurorestorative effects of neuregulins in the injured and aged dopaminergic nigrostriatal system." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1288981932.
Повний текст джерелаBacon, Gregory. "The anatomical basis for 5-HT-dopamine interactions in the rat substantia nigra and ventral tegmental area." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249483.
Повний текст джерелаWhyte, Kathryn Antonia. "Investigation of non-cholinergic acetylcholinesterase, and related peptides in an in vitro preparation of the substantia nigra." Thesis, University of Oxford, 2001. http://ora.ox.ac.uk/objects/uuid:967be89b-1b57-4d56-98de-70b4376ba1b3.
Повний текст джерелаBraitmaier, Helmine [Verfasser]. "Genetische Analyse der Echogenität der Substantia nigra und des gestörten Eisenstoffwechsels bei der Parkinsonschen Krankheit / Helmine Braitmaier." München : Verlag Dr. Hut, 2011. http://d-nb.info/1012432343/34.
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