Teses / dissertações sobre o tema "Neurones NPY"
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King, Peter John. "The study of NPY neurones in the rat hypothalamus". Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367248.
Texto completo da fonteLeclerc, Clémence. "Caractérisation multiparamétrique des neurones du hilus du gyrus denté chez la souris". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00833326.
Texto completo da fonteFioramonti, Xavier. "Mise en évidence et caractérisation de neurones sensibles au glucose dans le noyau arqué de souris : approche in vitro par électrophysiologie et étude in vivo". Toulouse 3, 2005. http://www.theses.fr/2005TOU30139.
Texto completo da fonteGlucose is known to regulate energetic homeostasis in controlling the electrical activity of glucose-sensing neurones. Using electrophysiological recordings on mouse brain slice, we show that 4 distinct glucose-sensitive neurones subpopulations exist in the arcuate nucleus. GE and GI neurones are respectively excited and inhibited by a hypoglycaemia (5-0 mM glucose); HGE and HGI neurones are respectively excited and inhibited by a hyperglycaemia (5-20 mM glucose). Then, in order to suggest a physiologic relevance of these neurones, we decided to characterize the neuropeptides express in these cells. Using NPY-GFP mouse, we show that GI neurones express NPY. Nevertheless, using POMC-GFP mouse, we show that GE or HGE neurones do not express POMC. This result was confirmed in vivo, in using the neuronal activating marker c-fos. This work replaces these glucose-sensitive neurones in the neural network involved in the control of energetic homeostasis
Mounien, Lourdes. "Etude du rôle des neurones à POMC du noyau arqué dans le contrôle de la prise alimentaire : Relations avec les systèmes neuropeptidergiques à NPY et à PACAP". Rouen, 2006. http://www.theses.fr/2006ROUES018.
Texto completo da fonteThe food intake is under control of a complex regulation mechanism involving several hypothalamic neuropeptides. Among them, neuropeptide Y (NPY) is orexigenic whereas α-melanocyte-stimulating hormone (α-MSH), a peptide generated by processing of proopiomelanocortin (POMC), and pituitary adenylate cyclase-activating polypeptide (PACAP) reduce food consumption. We have investigated the neuroanatomic and functional relations between POMC neurons of arcuate nucleus and the NPY and PACAP neuropeptidergic systems. Our data provide additionnal evidence for the function of arcuate POMC neurons in the regulation of energy homeostasis. Thus, it appears that POMC neurons are able to directly control the activity of the arcuate NPY system and that they are subjected to modulation by PACAP
Qu, Mengdi. "Molecular mechanism underlying CaMK1D-dependent function in AgRP neurons". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ029.
Texto completo da fonteDisruption of stress response mechanisms in organisms can lead to cellular dysfunction and diseases like metabolic syndrome. Energy balance is mainly regulated by the central nervous system (CNS), which integrates hormonal, neuronal, and dietary signals from various tissues. Dysfunction in this system is linked to obesity and metabolic syndrome, both precursors to type 2 diabetes (T2D). Our laboratory discovered that calcium/calmodulin-dependent protein kinase ID (CaMK1D), a gene associated with T2D, promotes ghrelin-mediated food intake in mice. However, CaMK1D signaling in NPY/AgRP neurons still remains questions. In this work, we proformed RNA sequencing using the GT1-7 hypothalamic cell line. To this end, we found that CalHM6 is a downstream target of CaMK1D signaling. CalHM6 mRNA levels were significantly upregulated in CaMK1D-/- cells and downregulated when CaMK1D was re-expressed. This was confirmed in vivo in the hypothalamus of CaMK1D-/- mice. CalHM6, likely a voltage-gated calcium channel, showed increased intracellular Ca2+ levels in response to ghrelin in CaMK1D-/- cells compared to CaMK1D+/+ cells using jGCamps method. Altogether, our work showed CalHM6 is a novel target of CaMK1D. High CaMK1D, leading to low CalHM6 expression, may enhance food intake and obesity by modulating calcium-dependent signaling in NPY/AgRP neuron
Joly, Aurélie. "Rôle du système nerveux dans le développement du syndrôme métabolique : étude de l'effet du glucose portal sur la sensibilité à l'insuline chez le rat : implication des neurones NPY/AgRP dans le contrôle de la balance énergétique chez la souris". Paris 7, 2011. http://www.theses.fr/2011PA077091.
Texto completo da fonteSeveral neuronal populations are involved in the regulation of energy balance. Among these, the hypothalamic agouti-related protein neurons (AgRP-neurons) are well characterized for their ability to promote food intake. Using cell-specific ablation we investigated a possible role of AgRP neurons in nutrient partitioning independent from food intake. We show that mice lacking AgRP neuron developed a non-hyperphagic obesity due to increased feed efficiency (weight gain/kcal consumed) on regular chow. At a time that preceded obesity catecholamine turnover rate was selectively decreased in the pancreas, liver, and glycolytic muscle, while it was increased in oxidative muscle. Respiratory quotient measurements revealed a change in substrate utilization towards lipid oxidation enhanced by synergistic increase in liver triglyceride synthesis and lipid substrate preference in oxidative muscle mitochondria. On high fat diet, mice lacking AgRP neurons displayed reduced body weight gain and paradoxical improvement in glucose tolerance. Finally we evidenced that Gamma Aminobutyric Acid (GABA) made by AgRP neurons is important in the central control of peripheral substrate utilization. This study reveals a new function for AgRP neurons in the coordination, via the sympathetic nervous System, of inter-organs communication and nutrient partitioning. These results offer a new conceptual framework for the understanding of obesity-related disorders
Lapray, Miroslawa. "Role of intercalated and NPY-expressing cells in neuronal circuit of the amygdala". Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:91017ce3-7c42-4310-94fb-be659ec2e52e.
Texto completo da fonteSt-Pierre, Jacques-André. "Cellular and pharmacological characterization of NPY YI receptor expression in cultured rat hippocampal neurons and astrocytes". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36838.
Texto completo da fonteThe present thesis examines the presence of NPY receptors in primary dissociated hippocampal cells in culture using a combination of molecular, pharmacological and immunocytochemical approaches. Receptor binding experiments revealed the preferential expression of Y1-like receptors over the Y2, Y4 and Y5 subtypes in rat hippocampal cultures. Cultured hippocampal cells expressed high level of Y1 receptors and very low amounts (below detection) of the Y2, Y 4 and Y5 receptor binding sites. The genuine nature of the Y1-like receptor expressed in these cells was confirmed using amplification (RT-PCR) of Y1 receptor mRNAs. The cellular phenotype expressing Y1 receptor was investigated using double labeling methods. Specific autoradiographic and immunolabeling signals of Y1-like receptors were observed on neurons (70% of the total population of neurons) and astrocytes (20% of the total population of glia cells) as revealed respectively by neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) immunostaining. The Y1 receptor labeling is distributed uniformly over neuronal cell bodies and processes compared to a non-uniform and clustered distribution on type I astrocytes. Neurons labeled by the various Y1 receptor markers were mostly glutamate-positive as revealed by double labeling. Interestingly, a small proportion (2--5%) of NPY-positive hippocampal neurons (NPY-positive cells represent around 10% of the total population of neurons) were also enriched with Y1 receptor labeling. These results suggest the possible autoregulatory role for the Y1 receptor on NPY release.
Taken together, these anatomical and pharmacological results suggest that Y1 receptor may play an important role in the hippocampus via the regulation of astrocytic and/or neuronal functions and the modulation of the release of glutamate and/or NPY.
Thiaw, Lamine Madani Kurosh. "Identification de systèmes dynamiques non-linéaires par réseaux de neurones et multimodèles". S. l. : S. n, 2008. http://doxa.scd.univ-paris12.fr:8080/theses-npd/th0407109.pdf.
Texto completo da fonteIdoux, Erwin. "Propriétés électrophysiologiques intrinsèques et modélisation des neurones responsables de l'intégration mathématique dans le noyau prepositus hypoglossi". Paris 6, 2007. http://www.theses.fr/2007PA066030.
Texto completo da fonteThe rationale behind this thesis is the understanding of the neural mechanisms involved in the mathematical integration of a velocity signal into a position signal. For eye movements in the horizontal plane, neurons of the prepositus hypoglossi nucleus (PHNn) are responsible for this integration. Here, PHNn have been classified in 3 types (A, B and D) according to their electrophysiological profile and then modeled. Unlike type A and B neurons, which are also found in the medial and lateral vestibular nuclei, type D neurons are specific to the NPH and their membrane potential shows subthreshold oscillations. Besides, persistent sodium conductance is crucial to the electrophysiology of the PHNn, however its impact and location are type-dependant. The intrinsic properties of neurons of the PHN and the vestibular nuclei have been compared to understand the link between the functions of these nuclei and the specific intrinsic properties of their respective neurons
Sene, Moustapha Madani Kurosh. "Contribution à la mise au point de techniques de détection et de diagnostic de défauts de roulements basées sur la tranformée en ondelettes et les réseaux de neurones artificiels". Créteil : Université de Paris-Val-de-Marne, 2008. http://doxa.scd.univ-paris12.fr:8080/theses-npd/th0405762.pdf.
Texto completo da fonteThèse uniquement consultable au sein de l'Université Paris 12 (Intranet). Titre provenant de l'écran-titre. Bibliogr. : 105 réf.
Dionisi, Marianna. "Involvement of ionic channels in chemically-induced neurotoxicity: examples of different molecular mechanisms". Doctoral thesis, Università del Piemonte Orientale, 2020. http://hdl.handle.net/11579/114773.
Texto completo da fonteRocha, Mariana Botelho da. "Autophagy in the hypothalamus: role of Neuropeptide Y and impact on Synaptic Plasticity". Doctoral thesis, 2016. http://hdl.handle.net/10316/29288.
Texto completo da fonteO hipotálamo é uma região do cérebro que regula o desenvolvimento, o crescimento e o metabolismo. Recentemente, foi também demonstrado que o hipotálamo desempenha um papel chave no desenvolvimento generalizado do envelhecimento. A autofagia é um processo intracelular envolvido na reciclagem dos constituintes da célula e na manutenção da homeostase celular. Durante o envelhecimento e em doenças associadas ao envelhecimento ocorre diminuição da autofagia. Por outro lado, em diversas espécies de animais, a restrição calórica (RC) é uma robusta intervenção anti-envelhecimento, aumentando o tempo de vida e diminuindo a incidência de doenças associadas à idade. A RC estimula a autofagia e também aumenta os níveis do neuropeptídeo Y (NPY) no hipotálamo. Diversos trabalhos mostram que o NPY tem um papel neuroprotector, aumenta a resistência ao stress. Contudo, o papel do NPY na autofagia nunca foi investigado. Desta forma, o primeiro objectivo deste trabalho foi estudar o papel do NPY na autofagia em neurónios do hipotálamo. Os resultados mostraram que o NPY estimula a autofagia numa linha de neurónios hipotalâmicos de murganho (mHypo-N42) e também em culturas primárias de células hipotalâmicas neurais diferenciadas de rato. O NPY aumentou o fluxo autofágico em neurónios do hipotálamo através da activação dos receptores Y1 ou Y5, e que activam as vias de sinalização intracelular PI3K, ERK e PKA. O efeito do NPY na autofagia num modelo in vivo também foi avaliado, através da sobre-expressão do NPY no núcleo arqueado do hipotálamo de murganhos C57BL/6, pela tecnologia de transferência génica usando vírus adenoassociados. Os resultados mostraram que o NPY também estimula a autofagia no hipotálamo in vivo. O núcleo arqueado do hipotálamo, responsável pela homeostase energética, é composto por duas populações neuronais distintas – neurónios que expressam POMC e CART, e neurónios que expressam NPY e AgRP. Estas duas populações regulam o anabolismo e catabolismo, recebendo e integrando sinais nutricionais e hormonais da periferia. Estudos recentes sugerem que a plasticidade sináptica dos circuitos hipotalâmicos envolvidos na ingestão alimentar também tem um papel na regulação da homeostase energética. Contudo, o papel da autofagia na plasticidade dos circuitos hipotalâmicos nunca foi investigado. Desta forma, o segundo objectivo deste trabalho foi investigar o papel da inibição específica de uma proteína fundamental do processo de autofagia, a Atg7, na organização sináptica, com uma dieta normal e em privação de alimentos. Os murganhos com inibição específica da proteína Atg7 nos neurónios POMC (POMC-Cre; Atg7loxP/loxP) foram usados como modelo animal de estudo e os murganhos com expressão inalterada de Atg7 (Atg7loxP/loxP mice) como controlos. Nestes animais avaliou-se a organização sináptica dos neurónios POMC. Os animais foram mantidos durante cerca de 10 semanas com acesso livre a uma dieta padrão ou sem acesso a comida durante uma noite. O núcleo arqueado do hipotálamo destes animais foi analisado por microscopia electrónica, microscopia de fluorescência e por microscopia óptica de luz visível. Os neurónios hipotalâmicos POMC dos murganhos POMC-Cre; Atg7loxP/loxP, com ausência de Atg7 nos neurónios hipotalâmicos POMC, apresentaram um aumento da área e do perímetro desses neurónios, e apresentaram acumulação de nematossomas. Além disso, os neurónios hipotalâmicos POMC dos murganhos POMC-Cre; Atg7loxP/loxP apresentaram mais contactos sinápticos, que se traduzem num aumento dos contactos simétricos inibitórios. Depois de uma noite sem acesso a comida, os neurónios do núcleo arqueado do hipotálamo dos murganhos POMC-Cre; Atg7loxP/loxP apresentaram menor imunorreactividade para c-Fos, que sugere menor activação neuronal. Em conclusão, os resultados desta tese mostram que o NPY induz o fluxo autofágico em neurónios do hipotálamo, e que a autofagia desempenha um papel na regulação da plasticidade sináptica dos neurónios POMC. Uma vez que a autofagia no hipotálamo e os níveis do NPY diminuem com o envelhecimento, a modulação do NPY pode ser um mecanismo protector contra a disfunção hipotalâmica associada ao aumento da idade. Por outro lado, a modulação da autofagia, através de um mecanismo sináptico subjacente, pode oferecer estratégias para a regulação do peso corporal.
The hypothalamus is the brain region that regulates development, growth and metabolism, and has gained increased attention for its key role in the progression of whole body aging. Additionally, autophagy, a highly regulated intracellular process involved in the turnover of most cellular constituents and in the maintenance of cellular homeostasis, is impaired in aging, contributing to the aging phenotype and to the aggravation of age-related diseases. On the other hand, caloric restriction (CR) is a robust anti-aging intervention, increasing lifespan and decreasing the incidence of age-related diseases. CR increases autophagy in different brain areas and increases neuropeptide Y (NPY) levels in the hypothalamus. Moroever, NPY has neuroprotective effects and increases resistance to stress and mean lifespan. However, the role of NPY on autophagy has never investigated before. Therefore, the first aim of this study was to investigate the role of NPY on autophagy in hypothalamic neurons. The results show that NPY stimulated autophagy in mouse hypothalamic cell line N42 (mHypo-N42) and also in rat differentiated hypothalamic neural cell cultures. Moreover, NPY stimulated the autophagic flux in hypothalamic neurons by activating NPY Y1 or Y5 receptors, through PI3K, ERK and PKA intracellular signaling pathways. We also evaluated the role of NPY on autophagy in vivo, by overexpressing NPY in the arcute nucleus (ARC) of hypothalamus of C57BL/6 mice, using adenoassociated viral (AAV) gene transfer technology. The results show that NPY also stimulated autophagy in hypothalamus in vivo. The hypothalamic ARC, responsible for energy homeostasis, is composed by two major neuronal populations – cocaine- and amphetamine-regulated transcript (CART)/Pro-opiomelanocortin (POMC) expressing neurons and agouti-related peptide (AgRP)/ neuropeptide Y (NPY) expressing neurons. These two neuronal populations regulate anabolic and catabolic state, receiving and integrating peripheral nutritional and hormonal signals. Recent observations suggest that synaptic plasticity in the hypothalamic feeding circuits has also a critical role in regulation of energy homeostasis, since the neuronal synaptic input organization in the hypothalamus is able to adapt and rearrange rapidly in response to metabolic hormones. In addition, autophagy in the hypothalamus was identified as a player in metabolic regulation. However, a role for autophagy in plasticity of hypothalamic feeding circuits has not been explored. Therefore, the second aim of this study was to investigate the role of Atg7 deletion in POMC neurons in the synaptic organization in mice under standard diet and food deprivation. POMC-specific Atg7 knockout mice (POMC-Cre; Atg7loxP/loxP) were used as animal model and Cre-negative Atg7loxP/loxP mice as controls, to evaluate the synaptic organization of the hypothalamic POMC neurons and neuronal activation in hypothalamic ARC. Animals were maintained during 10 weeks with standard diet or overnight fasting, and then brains slices containing arcuate nucleus of the hypothalamus were stained for electron microscopy and for fluorescence and light microscopy. The specific Atg7 deletion in POMC neurons resulted in an increased cell area and perimeter, and nematosomes accumulation. Moreover, we observed that POMC-Cre; Atg7loxP/loxP neurons have more synaptic inputs and more symmetric, putatively inhibitory inputs. After an overnight fasting, POMC-specific Atg7 knockout mice show no normal adaptation to food deprivation, with an impaired neuronal activation in hypothalamic ARC. Overall, these results show that NPY induces autophagic flux in hypothalamic neurons, and that autophagy has a role in the control of synaptic plasticity of POMC neurons. Since both hypothalamic autophagy and NPY levels decrease with age, modulation of NPY may act as a protective mechanism against impaired hypothalamic dysfunction associated with age. Moreover, autophagy modulation, through underlying synaptic mechanism, might offer strategies to the body weight regulation.
FCT - SFRH/BD/73004/2010
Faria, Paulo Jorge Félix. "Impact of emergent new psychoactive substances (NPS) on neuronal and microglial function". Master's thesis, 2020. http://hdl.handle.net/10362/111127.
Texto completo da fonteLin, Hung-Jui, e 林宏叡. "FGF8 from iPS-NPC enhances EPC motility to protect neuron cells". Thesis, 2011. http://ndltd.ncl.edu.tw/handle/70499811336842796937.
Texto completo da fonte國立陽明大學
微生物及免疫學研究所
99
Cerebrovascular disease resulting in stroke is a common cause of morbidity and mortality. In Taiwan, stroke is the third cause of death. Until now, we still don’t have a therapy that can cure stroke efficiently. The responses in brain after stroke are involves in lots of pathophysiological mechanism such as excitotoxicity, free radical damage, and inflammation. It is difficult to recover such injury via single therapy. The stem cell therapies are based on the differential potential of stem cell to achieve the purpose of tissue replacement. Beside, lots kind of stem cells have been reported having the neuroprotective capacity. Recent study implies that angiogenesis have an important role in brain tissue replacement and the endothelial progenitor cell (EPC) predominant angiogenesis in adult especially in pathological condition. In this study, we first performed the migration assay of endothelial cell to evaluate the angiogenic capacity of variant stem cells. Then we demonstrated that induced-pluripotency stem cell derived neural progenitor cell (iPSN) can secret FGF8 to attract EPC and promote angiogenesis and iPSN induce angiogenesis in MCAO rat as well. Further, downstream of FGF8 the ERK signal is essential for EPC angiogenesis. Additionally, we prove that EPC have more neuroprotective capacity then mature endothelial cell in vitro.
Muñoz, Rios Erith Alexander. "Determinación de Tasa de Precipitación a partir de datos ATMS mediante un algoritmo basado en Redes Neuronales Artificiales". Master's thesis, 2014. http://hdl.handle.net/11086/11523.
Texto completo da fontePeake, Kyle. "Cholesterol metabolism in the Niemann-Pick Type C brain". Phd thesis, 2011. http://hdl.handle.net/10048/1696.
Texto completo da fonteExperimental Medicine
Shih, Kun-syong, e 施焜雄. "Effect of H-PLGA NPs on the ElectrophoreticMobility and Zeta Potential of Rat Bone Marrow Stromal Cells in the Process of Differentiation into Neuron". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/75822785802264196525.
Texto completo da fonte國立中正大學
化學工程所
96
The purse of the study was to investigate the electrophoretic mobility and zeta potential of rat bone marrow stromal cells (rBMSCs) with different concertration of neuron growth factor (NGF) at various induced time, heparin loading poly (D,L lactide-co-glycolide) nanoparticles (H-PLGA NPs) prepared by different ratio of surfactant (lecithin/Tween 80) with various concertration of heparin and rBMSCs coculture with various heparin loading efficiency H-PLGA NPs at various induced time. The size of H-PLGA NPs were measured by zetasizer and confirmed by the images of FE-SEM and TEM. The fixed charge density of rBMSCs were estimated from the electrophoretic mobility of capillary electrophoresis with the soft particle electrokinetic theory. The result revealed that, the ratio of lecithin and the concertration of heparin increased, the size and the absolute value of electrophoretic mobility and zeta pontential of H-PLGA NPs increased. The absolute value of electrophoretic mobility and zeta pontential of rBMSCs increased with an increase of induced time in the process differentiation into neuron. The weight of H-PLGA NPs uptaked by rBMSCs inereased with an increase of heparin loading efficiency of H-PLGA NPs. The absolute value of electrophoretic mobility and zeta pontential of rBMSCs decreased with an increase of rBMSCs uptakes H-PLGA NPs in the process differentiation into neuron.