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1
Cavallari, Paolo. "Organisation des circuits transmettant inhibition et excitation entre les muscles antagonistes du poignet chez l'homme." Paris 6, 1988. http://www.theses.fr/1988PA066126.
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Djabali, Karima. "Dynamiques et interactions specifiques de la peripherine, proteine de filament intermediaire neuronale." Paris 7, 1991. http://www.theses.fr/1991PA077161.
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La peripherine, proteine neuronale de filament intermediaire de type iii est co-exprimee avec les neurofilaments dans certaines populations neuronales et avec la vimentine dans les lignees de neuroblastome. Nous avons montre que la peripherine est co-localisee avec les neurofilaments dans les neurones de ganglions sympathiques et sensoriels ainsi qu'avec la vimentine dans des cellules de neuroblastome. Nous avons etudie les interactions moleculaires entre la peripherine et les lamines nucleaires. Nous avons montre que la peripherine purifiee interagit specifiquement in vitro avec la lamine b de mammifere. Nous avons egalement demontre qu'un peptide synthetique (pi) representant la partie proximale du domaine carboxy-terminal de la peripherine est aussi capable d'association avec la lamine b de maniere specifique et saturable et de facon cooperative. Des animaux de laboratoire immunises avec le peptide i developpent spontanement des anticorps idiotypiques et anti-idiotypiques capables de reconnaitre respectivement la peripherine et la lamine b. Ces resultats demontrent in vivo que la lamine b est le recepteur nucleaire de la peripherine
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Giasson, Benoit I. "Regulatory and aberrant phosphorylation of neuronal intermediate filament proteins." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37546.
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The activation of cyclic AMP-dependent protein kinase (PKA) in rat dorsal root ganglion (DRG) cultures, treated concomitantly with low concentrations of okadaic acid that selectively inhibit protein phosphatase-2A, enhanced the disassembly of neuronal intermediate filaments (IFs). The latter disassembly correlated with phosphorylation of the peripherin head domain and a novel, identified PKA site, Ser-2, in the low molecular mass neurofilament (NF) subunit (NFL). On the other hand. insignificant levels of 32P were incorporated into alpha-internxin under control and experimental conditions that promote disassembly. These findings indicate that phosphorylation of the latter protein is not directly involved in the fragmentation of neuronal IFs Phosphopeptide mapping of the mid-size (NF) subunit (NFM) revealed that 32P-labelling of one of its many phosphopeptides is correlated with neuronal IF fragmentation.<br>The expression and Triton X-100 (Triton) solubility of neuronal IF proteins were determined in the developing rat cerebral cortex. The level of expression of alpha-internexin was unchanged from embryonic day 15 (E15) to postnatal day 15 (P15), whereas expression of (NF) subunits increased during this time interval. NFL was largely insoluble in Triton from the time, P5, when there were sufficient amounts for its solubility to be assayed. There was a continual reduction in the Triton solubility of NFM and alpha-internexin during the E15-P15 developmental period. Similar expression patterns and Triton solubility profiles were obtained for neuronal IF proteins in cultured neurons from E15 cerebral cortex. These results suggest that alpha-internexin is expressed earlier than (NF) proteins to provide a more plastic network in the early developing brain.<br>Correlative studies and direct, in vivo activation of stress-activated protein kinases (SAPKs) were used to demonstrate that SAPKs are involved in aberrant phosphorylation of the perikaryal high molecular mass (NF) subunit (NFH). It was also shown that hyperphosphorylation of perikaryal NFH is a reversible process that does not involve p38 kinases or extracellular signal-regulated kinases (ERKs). The use of defined peptide substrates indicated that SAPKgamma preferentially phosphorylates KSPXE motifs in NFH. SAPKgamma was shown to be located both in the cell body and neurites of cultured DRG neurons, suggesting that it is likely to be involved in the phosphorylation of cytoplasmic proteins. Collectively, these findings strongly support the notion that activation of SAPKs causes the aberrant hyperphosphorylation of perikaryal NFH reported in many neurological diseases.
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Giasson, Benoit I. "Regulatory and aberrant phosphorylation of neuronal intermediate filament proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0003/NQ44440.pdf.
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Mosaheb, Sabrina. "Investigations of neuronal Pin1 protein in neurodegeneration, focusing on neuronal intermediate fillament inclusion disease." Thesis, University of Sussex, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488585.
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Following reports that in Alzheimer's disease (AD) Pin I associates with intraneuronal neurofibrillary tangles (NFTs; a hallmark pathological feature), Pin I has become a protem of interest in this disorder.
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ESCURAT, MICHEL. "Etude de l'expression dynamique de la peripherine, proteine constitutive de filament intermediaire neuronale." Paris 6, 1992. http://www.theses.fr/1992PA066137.
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Cette these represente une etude de l'expression de la peripherine, proteine neurospecifique constitutive de filament intermediaire de type iii. Trois types de recherches ont ete abordees: 1) l'etude de sa distribution spatio-temporelle de la peripherine comparee a celle de la proteine de neurofilament nf-l au cours du developpement chez le rat; 2) l'effet de l'environnement cellulaire sur l'expression de cette proteine; 3) l'effet de l'inhibition de son expression. Il en resulte que l'expression de la peripherine est contemporaine de celle de nf-l mais qu'elle reste limitee a certaines populations neuronales. Sa distribution ne depend ni d'une origine embryonnaire commune, ni d'une fonction neuronale particuliere. En effet, le seul point commun aux differents neurones exprimant la peripherine est qu'ils projettent tous leurs neurites a l'exterieur de l'axe encephale-moelle epiniere. Cette distribution pourrait donc dependre d'elements epigenetiques associes a l'environnement glial; et peut laisser supposer que cette proteine interviendrait dans la dynamique d'extension neuritique. L'etude in vivo et in vitro de la modulation de l'expression de la peripherine en fonction de l'exposition de differents neurones a divers environnements cellulaires a revele que l'expression de cette proteine pouvait etre induite par la presence de fibroblastes. Les observations obtenues lors de l'etude de l'inhibition de son expression, a l'aide d'oligodeoxynucleotides antisens, dans des neurones sensoriels en culture ne permettent pas actuellement de confirmer ou d'infirmer l'hypothese de l'extension neuritique
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Larivière, Roxanne. "Transgenic approach to study the role of intermediate filaments in motor neuron disease." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84279.
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Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disorder characterized by the loss of upper and lower motor neurons. Many reports lead to the hypothesis that a high axonal neurofilament burden and a large axonal caliber account for the selective vulnerability of motor neurons affected in ALS (Kawamura et al., 1981; Sobue et al., 1981; 1987). Transgenic mice expressing a mutant form of SOD1-linked to familial ALS and having one disrupted allele for each neurofilament gene were generated to address this issue. Despite a 40% reduction in neurofilament content and a decrease of large axonal caliber from 5--9 mum to 1--5 mum, these mice did not show an extended life span, nor did they display an alleviated loss of motor axons. These results do not support the idea that high neurofilament content and large axonal caliber are responsible for the selective vulnerability of motor neurons in ALS.<br>Peripherin, a type III intermediate filament (IF) protein is also expressed in spinal motor neurons, and is present together with neurofilaments in axonal spheroids of ALS patients, suggesting that this protein could be involved in the pathogenesis of ALS. Moreover, mice overexpressing a peripherin transgene develop a late-onset motor neuron death characterized by the presence of IF inclusion bodies (Beaulieu et al., 1999a). In a first attempt to clarify the role of peripherin in ALS, peripherin knockout mice were generated. Peripherin null mice were viable, reproduce normally and did not exhibit overt phenotype. However, they did show a 34% reduction in the number of L5 unmyelinated sensory fibers demonstrating a requirement of peripherin for the proper development of a subset of sensory neurons.<br>Finally, in order to investigate whether peripherin contributes to the pathogenesis of ALS, mutant SOD1 mice were generated in a peripherin overexpressing background and a peripherin depleted background. Unexpectedly, upregulation or suppression of peripherin expression had no effect on disease onset, mortality and motor neuron loss in mutant SOD1 mice. Taken together, these results provide compelling evidence that peripherin is not a key contributor of motor neuron degeneration associated with toxicity of mutant SOD1.
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Yazdani, Armin A. "The Smn-Independent Beneficial Effects of Trichostatin A on an Intermediate Mouse Model of Spinal Muscular Atrophy." Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30703.
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Trichostatin A (TSA) is a histone deacetylase inhibitor with beneficial effects in spinal muscular atrophy mouse models that carry the human SMN2 transgene. Whether TSA specifically targets the upregulation of the SMN2 gene or whether other genes respond to TSA and in turn provide neuroprotection in SMA mice is unclear. We have taken advantage of the Smn2B/- mouse model that does not harbor the human SMN2 transgene, to test the hypothesis that TSA has its beneficial effects through a non-Smn mediated pathway. Daily intraperitoneal injection of TSA from postnatal day 12 to 25 was performed in the Smn2B/- mice and littermate controls. Previous work from our laboratory demonstrated that treatment with TSA increased the median lifespan of Smn2B/- mice from twenty days to eight weeks. As well, there was a significant attenuation of weight loss and improved motor behavior. Pen test and righting reflex both showed significant improvement, and motor neurons in the spinal cord of Smn2B/-mice were protected from degeneration. Both the size and maturity of neuromuscular junctions were significantly improved in TSA treated Smn2B/- mice. Here, we have shown that TSA treatment does not increase the levels of Smn protein in mouse embryonic fibroblasts or myoblasts obtained from the Smn2B/- mice. Further, qPCR analysis revealed no changes in the level of Smn transcripts in the brain or spinal cord of TSA-treated SMA mice. Similarly, western blot analysis revealed no significant increase in Smn protein levels in the brain, spinal cord, hind limb muscle, heart muscle, or the liver of TSA treated Smn2B/- mice. However, TSA has beneficial effects in the muscles of Smn2B/- mice and improves motor behavior and myofiber size. TSA improves muscle development by enhancing the activity of myogenic regulatory factors independent of the Smn gene. The beneficial effect of TSA is therefore likely through an Smn-independent manner. Identification of these protective pathways will be of therapeutic value for the treatment of SMA.
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Bahia, Parmvir Kaur. "A study of small and intermediate conductance calcium-activated potassium channels in sensory neurones." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445301/.
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The role of small and intermediate conductance calcium-activated potassium channels (SK and IK channels) in dorsal root ganglion (DRG) neurones was examined. Sixteen antibodies raised against human or rat SK/IK channel peptide epitopes were tested for their ability to stain cells expressing channel protein. Of sixteen antibodies, 12 (6 to SKI, 1 to SK2, 2 to SK3 and 3 to IK) were deemed suitable for immunohistochemistry in human or rat tissue. Real-time quantitative PCR (qPCR) of rat DRG cDNA was performed to examine SK/IK expression levels. DRG neurones produce mRNA for all SK/IK channels and these mRNA levels were found to increase during development. Antibody staining experiments using DRG neurones cultured from different aged animals produced a positive stain with the anti-SK3 antibody only. The number of cells that stained positively and the intensity of staining for SK3 increased with age. To investigate possible functional roles for SK/IK channels sensory neurones, action potential afterhyperpolarisations (AHPs) were recorded from cultured DRG and nodose cells. The majority of these AHPs proved to be insensitive to the SK channel blocker UCL 1848. Attempts to block medium duration AHPs in DRG cells using IK and calcium channel blockers, also failed in most cases, suggesting that some other potassium conductances) are responsible. The possibility that SK3 is functional at the terminals of primary afferents was examined next. Spinal cord slices stained with SK/EK channel antibodies revealed positive SK3 staining in the outer laminae of the dorsal horn, where small and large diameter DRG fibres are expected to terminate. In vivo experiments (done by Dr Rie Suzuki, Department of Pharmacology, UCL) using UCL 1848 and l-ethyl-2- benzimidazolinone (1-EBIO an SK channel opener) showed that SK channels are likely to be active at these terminals where they have a functional role in mediating innocuous mechanical and nociceptive responses.
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Athlan, Eric S. "Study of in vivo and in vitro associations between neuronal intermediate filament proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq44352.pdf.
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Doroudchi, Mohammad Mehdi. "Modification of intermediate filaments in motor neurons and other cells by activation of protein kinase C." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40341.
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The effects of activation of protein kinase C (PKC) on intermediate filaments (IFs) of different cell types were investigated. In primary cultures of murine or rabbit spinal cord, or human fibroblasts, brief exposure to activators of PKC led to the following changes in IFs: (1) Disassembly of GFAP-filaments in astrocytes and of vimentin in fibroblasts and fragmentation of the neurofilament (NF) network in neuronal cell bodies (occurred within 30 minutes). The distribution of PKC isoforms was investigated in these cell types and no IF-associated isoform was found. Disassembly of IFs may be explained by direct phosphorylation of N-terminal domains of IFs by PKC. (2) Activation of PKC led also to changes similar to those occurring in various motor neuron diseases: Focal swellings of proximal neurites of motor neurons, but not other types of neurons (within hours), and hyperphosphorylation of C-terminal domains of NF proteins (persisting over days). NF phosphorylation was determined by increased immunoreactivity with antibodies SMI31 and SMI34 recognizing NF proteins (NF-M & NF-H) when C-terminal KSP repeat domains are in intermediate and hyperphosphorylated states, respectively. Increased SMI34 labeling was prevented by pretreatment with the selective NMDA receptor antagonist, D-2-amino-5-phosphonovaleric acid (APV), but not by the AMPA/kainate antagonist, CNQX, or the metabotropic glutamate receptor antagonist, MCPG, indicating a cooperative effect of NMDA receptor activation in PKC-induced NF hyperphosphorylation. Since PKC does not phosphorylate C-terminal domains of NF proteins, involvement of other kinases was investigated. Hyperphosphorylation of NFs induced by PKC was prevented by the specific Ca$ sp{2+}$/calmodulin-dependent protein kinase II (CaMKII) inhibitor, KN-62, but not by its analogue, KN-04. The following mechanism is proposed for NF hyperphosphorylation in motor neuron diseases: Activation of PKC, as a nonspecific response to injury, acts cooperati<br>The results of the present thesis together demonstrate multiple effects of PKC activation on modulation of IFs that might contribute to dysfunction of cells in certain diseases.
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Johansson, Clas B. "Isolation and characterization of adult neural stem cells /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-104-7/.
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ZHANG, ZHONG-WEI. "Mise en evidence de recepteurs cholinergiques nicotiniques de type neuronal dans les cellules endocrines de lobe intermediaire de l'hypophyse." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR13031.
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Notre travail s'inscrit dans le cadre d'une etude de la regulation de la fonction de l'hypophyse par le systeme nerveux central. Par la technique du patch-clamp, nous avons etudie les reponses a l'acetylcholine (ach) dans les cellules du lobe intermediaire (li) de l'hypohyse de porc. Nos resultats montrent que ces reponses sont bloquees par la d-tubocurarine, l'hexamethonium, la mecamylamine, et sont insensibles a alpha-bungarotoxine. Ces propriete sont caracteristiques d'un recepteur nicotinique de l'ach de type neuronal. L'effet excitateur de l'ach passe par une activation du canal ionique constitutif du recepteur de l'ach. Ce canal possede une conductance elementaire de 26 ps et une duree moyenne d'ouverture de 1. 8 ms. Nous avons montre enfin que la bicuculline, l'antagoniste selectif du recepteur gaba-a, bloque egalement la reponse cholinergique nicotinique des cellules du li. En conclusion, nos resultats montrent la presence d'un recepteur nicotinique de type neuronal au niveau des cellules du li et suggerent un role de l'ach dans la regulation de la fonction endocrine de ces cellules hypophysaires
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Ogura, Takenori. "Three-dimensional induction of dorsal, intermediate and ventral spinal cord tissues from human pluripotent stem cells." Kyoto University, 2019. http://hdl.handle.net/2433/236613.
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ROBERT, PATRICK. "Effets de l'accumulation des filaments intermediaires sur la biologie des neurones chez des souris transgeniques exprimant une proteine de fusion nfh--galactosidase." Rennes 1, 2000. http://www.theses.fr/2000REN10034.
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L'expression d'une proteine de fusion entre la sous-unite lourde des neurofilaments et la -galactosidase chez des souris transgeniques provoque l'agregation des filaments intermediaires neuronaux dans le corps cellulaire et leur absence du compartiment axonal. Ces souris presentent des similitudes avec des neuropathologies et constituent un modele d'etude des effets de la desorganisation cytosquelette neuronal. L'expression des genes du cntf, cntf-r, ngf, nt-3 et gapdh n'est pas modifiee demontrant que la production de facteurs neurotrophiques et l'activite de transcription basale des neurones n'est pas affectee par une desorganisation du cytosquelette. Le transgene est tres faiblement exprime par rapport a nfh endogene et peut s'expliquer par l'absence de sequences regulatrices comprises dans la sequence 3non traduite. Les taux d'arnm des neurofilaments et microtubules demeurent inchanges. La quantite de proteine de neurofilaments est reduite de 50% et signe l'activation d'une nouvelle voie de metabolisme, par contre celle des proteines de tubuline augmente de 25% demontrant que l'equilibre de polymerisation de la tubuline et donc de synthese est controlee par les neurofilaments. Les souris nfh-lacz sont caracterisees par une sur myelinisation axonale du systeme nerveux peripherique associee a une myelinisation normale des axones du systeme nerveux central. L'expression de certains genes de la myeline n'est pas modifiee chez les souris transgeniques. Le taux d'arnm de p 0 est diminue et semble etre lie a la composition de l'axosquelette. Les variations d'expression du gene plp entre le cerveau et la moelle epiniere indique l'existence de mecanismes de regulation differents au sein du systeme nerveux central. Les variations des taux d'arnm des genes de la myeline reflete l'influence de l'environnement genetique sur la biologie de la myeline. Ces resultats montrent que les accumulations de nf participent plus de la semiologie que de l'etiologie de certaines neuropathies.
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Poisbeau, Pierrick. "Etude electrophysiologique des controles excitateurs et inhibiteurs au niveau des cellules du lobe intermediaire de l'hypophyse en culture primaire ou en coculture avec des neurones hypothalamiques." Université Louis Pasteur (Strasbourg) (1971-2008), 1996. http://www.theses.fr/1996STR13034.
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Ce travail de these presente les caracteristiques d'un modele de synaptogenese neuroendocrinien entre des neurones hypothalamiques et des cellules du lobe intermediaire (li) de l'hypophyse de rat. Lorsque ces deux types cellulaires sont places en co-culture, on observe la mise en place de synapses gabaergiques. Cette mise en place est abordee par des techniques d'immunocytochimie, de microscopie electronique et d'electrophysiologie. Le gaba libere par les terminaisons des neurones hypothalamiques active les recepteurs gaba-a associes a une permeabilite aux ions chlorures. Les courants synaptiques gaba-a sont modulables par les barbituriques, les benzodiazepines et les neurosteroides. Parallelement a l'etude de cette synapse, la mise en evidence et la caracterisation d'un recepteur non-nmda du glutamate sur les cellules du li a ete realisee
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Najas, Sales Sònia 1985. "Role of DYRK1A in the development of the cerebral cortex : Implication in Down Syndrome." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/380895.
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In this work we have assessed the possible contribution of the human chromosome-21 gene DYRK1A in the developmental cortical alterations associated with Down Syndrome using the mBACTgDyrk1a mouse, which carries 3 copies of Dyrk1a, and a trisomic model of the syndrome, the Ts65Dn mouse. We show that trisomy of Dyrk1a changes the cell cycle parameters of dorsal telencephalic radial glial (RG) progenitors and the division mode of these progenitors leading to a deficit in glutamatergic neurons that persist until the adulthood. We demonstrate that Dyrk1a is the triplicated gene that causes the deficit in early-born cortical glutamatergic neurons in Ts65Dn mice. Moreover, we provide evidences indicating that DYRK1A-mediated degradation of Cyclin D1 is the underlying mechanism of the cell cycle defects in both, mBACTgDyrk1a and Ts65Dn dorsal RG progenitors. Finally, we show that early neurogenesis is enhanced in the medial ganglionic eminence of mBACTgDyrk1a embryos resulting in an altered proportion of particular cortical GABAergic neuron types. These results indicate that the overexpression of DYRK1A contributes significantly to the formation of the cortical circuitry in Down syndrome.<br>En aquest treball s'ha avaluat la possible contribució del gen DYRK1A, localitzat en el cromosoma humà 21, en les alteracions del desenvolupament de l’escorça cerebral associades a la Síndrome de down (SD) mitjançant l’estudi de dos models murins: el ratolí mBACTgDyrk1a, el qual conté 3 còpies de Dyrk1a, i el ratolí Ts65Dn, un dels models trisòmics de la SD més ben caracteritzats. Els nostres resultats mostren que la trisomia de Dyrk1A altera alguns paràmetres del cicle cel•lular i el tipus de divisió dels progenitors neurals del telencèfal dorsal, donant lloc a un dèficit de neurones glutamatèrgiques que persisteix fins l’edat adulta. Hem demostrat que Dyrk1a és el gen triplicat responsable del dèficit inicial en la generació de neurones glutamatèrgiques corticals observat en el ratolí Ts65Dn. A més a més, hem proporcionat evidències de que la degradació de Ciclina D1 induïda per DYRK1A és el mecanisme molecular subjacent a les alteracions de cicle cel•lular observades en els progenitors neuronals dels embrions mBACTgDyrk1a i Ts65Dn. Per altra banda, hem demostrat que la neurogènesis inicial està incrementada en l’eminència ganglionar medial dels embrions mBACTgDyrk1a, fet que altera la proporció de subtipus específics d’interneurones GABAèrgiques en l’escorça cerebral adulta. En conclusió, els nostres resultats indiquen que la sobreexpressió de DYRK1A contribueix significativament a la formació dels circuits cortical en la SD.
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Welin, Dag. "Neuroprotection and axonal regeneration after peripheral nerve injury." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32819.
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Kuang-Wen, Tseng. "The Role of Neuronal Intermediate Filament in the Dorsal Root Ganglion and Spinal Motor Neurons of Dystonia musculorum Mice." 2006. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-3011200610280500.
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Tseng, Kuang-Wen, and 曾廣文. "The Role of Neuronal Intermediate Filament in the Dorsal Root Ganglion and Spinal Motor Neurons of Dystonia musculorum Mice." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/36413409256207445291.
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博士<br>國立臺灣大學<br>解剖學研究所<br>95<br>Dystonia musculorum (dt) is a mutant mouse with hereditary neuropathy. A defective neuronal form of bullous pemphigoid antigen 1 (BPAG1n) gene is responsible for this mutation. Previous study indicated that BPAG1n is expressed in wide variety of neuronal tissues and is highly and consistently expressed in dorsal root ganglia (DRG) neurons, but it is reduced in spinal motor neurons. BPAG1n is one of the cytolinker proteins that could interact with neuronal intermediate filament (IF) proteins, such as α-internexin, peripherin and neurofilaments. In the present study, we examined the pathological role of IF proteins in DRG neurons and spinal motor neurons of dt mice by using different approaches.
In our pilot study, we found that not only BPAG1n but also α-internexin was absent in DRG neurons of adult dt mice. To study the relationship between the absence of α-internexin and the progressive neuronal loss in the DRG of dt mice, we further cultured DRG neurons from embryonic dt mutants. Immunocytochemical assay of cultured DRG neurons from dt embryos revealed that α-internexin was aggregated in the juxtanuclear cytoplasm and in the proximal region of axons, yet other IF proteins were widely distributed in all processes. Active caspase-3 activity was observed in the neurons with massive accumulation of α-internexin of dt mice. From our observations, we suggest that the interaction between BPAG1n and α-internexin may be one of the key factors involved in neuronal degeneration, and abnormal accumulation of α-internexin may impair the axonal transport and turn on subsequently the cascade of neuronal apoptosis in DRG neurons of dt mice.
Immunofluorescence staining revealed that α-internexin is a major component in the swelling axon, and that an abnormal translocation of α-internexin in the nucleus of spinal motor neuron in dt mice. This abnormal translocation of α-internexin in the nucleus of spinal motor neuron was also confirmed by Western blotting and immunoelectron microscopy. Cell death of spinal motor neurons was further tested by TUNEL assay, and no positive cells could be identified from spinal motor neurons in dt mice. All these results indicated that the spinal motor neuron, unlike the DRG neuron, keep surviving after accumulation of α-internexin in the swelling axon and abnormal translocation of α-internexin in the cell nucleus. We suggest the capacity of multipolar spinal motor neurons to resist the neuronal IF aggregation is better than that of DRG neurons.
In summary, we demonstrated that massive neuronal IFs accumulations result in the cell death of DRG neuron, but not in spinal motor neuron, in dt mutants and thus we conclude that the accumulations of neuronal IFs led to selective neuronal degeneration. The mechanism of the neuronal death after the accumulation of neuronal IFs remains to be elucidated.
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Shih, Meng-Fu Maxwell, and 施孟甫. "Anterior Paired Lateral Neurons in Drosophila Intermediate-Term Memory." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/35964851501713798698.
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博士<br>國立清華大學<br>生物科技研究所<br>102<br>The secrets of memory have tantalized people for centuries. Excitingly neuroscientists using fly Drosophila melanogaster as the model animal to study memory started to manipulate different forms of memory at different processing stages from genes or molecules to circuits. As more and more evidence accumulate a picture addressing how the memory is formed in the fly brain is getting complete. This dissertation reveals two additional roles of the anterior paired lateral (APL) neuron in the intermediate-term memory (ITM), in addition to the known role in olfactory learning. Gap junctions, or electrical synapses, are important for normal brain functions but their contribution to memory formation has not been well characterized. We have shown that two extrinsic neurons, the APL and DPM neurons, form gap-junctional communication in the mushroom body (MB), the learning and memory center in the fly brain. Fly olfactory associative conditioning produces two components of ITM: anesthesia-sensitive memory (ASM) and anesthesia-resistant memory (ARM). Following disruption with RNAi-mediated knockdowns of inx7 and inx6 in the APL and DPM neurons, respectively, we found that flies showed normal olfactory associative learning and intact ARM but could not form 3-h ASM. These data reveal that the heterotypic gap junctions between the APL and DPM neurons are an essential part of the MB circuitry for ASM, suggesting that a recurrent neural circuit, consisting of APL, DPM and MB neurons, may stabilize ASM within the MB. In addition to the gap-junctional role of the APL and DPM neurons in ASM, we also have shown that the chemical neurotransmission from the APL neurons, after conditioning but before testing, is necessary for ARM formation. Immunostaining and an adult-stage-specific RNAi knockdown indicated that octopamine from the APL neuron acts on MB α′β′ Kenyon cells (KCs) via Octβ2R octopamine receptors to modulate ARM formation. Surprisingly the serotoninergic DPM—αβ KCs pathway and the octopaminergic APL—α′β′ KCs pathway are additive for 3-h ARM, suggesting they modulate ARM formation in the MB in parallel.
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Liu, Tzu-Chiang. "Overexpression of neuronal intermediate filament internexin in the PC-12 cell line." 2004. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-1207200417002500.
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Liu, Chi-Hsiu, та 劉紀秀. "Molecular Cloning and Characterization of Chicken Neuronal Intermediate Filament Protein α-Internexin". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/82730612255472345215.
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博士<br>國立臺灣大學<br>解剖學暨生物細胞學研究所<br>101<br>α-Internexin is one of the neuronal intermediate filament (IF) proteins, which also include peripherin and neurofilament (NF) triplet proteins designated as NFL, NFM and NFH for low, middle and high molecular weight subunits, respectively. It is expressed by most neurons as the differentiation begins and precedes the expression of the NF triplet proteins in mammals. Unlike the NF triplets which are obligate heteropolymers, α-internexin has the ability to form homopolymers. These studies have supported the belief that α-internexin and NF triplet form separate filament systems. The chicken is an important model organism that bridges the evolutionary gap between mammals and other vertebrates. It also represents the first non-mammalian amnitoe to have its genome sequenced. The chicken embryo is a useful model system in developmental biology due to experimental advantages of in ovo embryogenesis. Some neuronal IF genes of chicken were cloned in previous studies. Still, little is known about the gene sequence and physiological function of the neuronal IF α-internexin in avian.
In this study, we aim to identify the mRNA sequence encoding chicken α-internexin and to characterize the gene structures and expression levels during developmental process. Human, mouse, rat, frog and zebrafish α-internexin sequences were used to search for orthologues. The putative chicken α-internexin (chkINA) cDNA was generated via RT-PCR of total chicken brain RNA. The gene structures and predicted amino acid sequence of chkINA revealed a high similarity with the homologues from human, mouse, rat, bovine, frog, and zebrafish. Transient transfection assay showed that the filamentous pattern of chkINA could be found in transfected cells, and colocalized with other endogenous IFs by demonstration of immunocytochemistry with chicken-specific antibody. The expression of chkINA was detected in early stage of development and during developmental process. Moreover, chkINA was widely expressed in chicken brains and retinae, and was colocalized in fibrous patterns with NF triplet proteins. chkINA was also expressed abundantly in the developing cerebellum and was the major IF protein in the parallel fibers of granule neurons. In addition, chkINA could be transiently detected in all neuronal lineages in the developing chicken retina; however, as development progressed, chkINA expression became restricted to the nerve fibers of ganglion, amacrine and horizontal cells. Thus, we conjecture that chkINA might be a neuron-specific IF protein and could be a useful marker to be applied to neurobiological studies in chicken. The annotation of chkINA may be applied for neuroscience research. In addition, this may fill the gaps of the molecular evolution of neural intermediate filaments, and provide hints in genomics, evolutionary developmental biology or bioinformatics.
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Liu, Tzu-Chiang, and 劉自強. "Overexpression of neuronal intermediate filament internexin in the PC-12 cell line." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/57299301444864791801.
Full textAbstract:
碩士<br>國立臺灣大學<br>解剖學暨細胞生物學研究所<br>92<br>The neuronal intermediate filaments include not only the neurofilament triplet proteins but also peripherin and internexin. Both peripherin and internexin are expressed in the neurons of PNS and CNS during development. To determine whether neurite outgrowth is enhanced by internexin, the cDNA of rat internexin tagged with EGFP was transfected into a rat adrenal pheochromocytoma cell line PC-12 that responds to nerve growth factor (NGF) by induction of the neuronal phenotype. After G418 selection, 5 stable cell lines were established. Selected stable clones were induced by NGF and examined for expression patterns of neuronal intermediate filaments by western blot and immunocytochemistry. Differentiating neurons were also collected after NGF induction for RT-PCR analyses.
Comparing the internexin-EGFP transfected stable cell line with non-transfected PC-12 cells, overexpressed internexin-EGFPs were found mainly in cell bodies and the proximal part of neurites. It was also found that overexpression of internexin-EGFPs enhanced the neurite outgrowth of PC-12 cells at the early stages of NGF induction. NF-L and NF-M were up-regulated by the overexpression of internexin-EGFPs. Interestingly, internexin-EGFP transfected cells detached from culture plates obviously at the later stages of NGF induction. Massive IF accumulations, swelling mitochondria, degenerating neurites with numerous electron-dense granules were observed ultrastructurally in the internexin-EGFP transfected cells. These observations may imply that cell death was undergoing in internexin-EGFP transfected cells.
From this study, it could be suggested that internexin may play an important role in the neurite outgrowth and regulate the expression of other neurofilaments during neuronal development. Apoptosis-like cell death could be also induced by the overexpression of internexin-EGFP in PC-12 cells after the NGF induction.
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Ko, Tsui-Ling, and 柯翠玲. "The Expression of Neuronal Intermediate Filaments in the Developing Mouse Epiphysis and Neurohypophysis." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/82921080274972600577.
Full textAbstract:
博士<br>國立臺灣大學<br>解剖學研究所<br>93<br>The mammalian epiphysis (pineal gland) and neurohypophysis (posterior lobe of pituitary gland) originated ependymal cell of the roof and the floor of the third ventricle from central nerve canal respectively. In certain species, the pineal gland contains neurons and/or neuron-like peptidergic cells, The nature and cytological features of these neuronal cells, in addition to the pinealocytes, interstitial cells need to be classified. Posterior pituitary consists of pituicytes, the modified astrocytes and the predominant cellular type in the neurohypophysis, Development and the role of pituicytes still has many aspects remain to be clarified so far; and axons, originating from neurons in supraoptic and paraventricular nuclei synthesizing vasopressin and oxytocin. The neuronal intermediate filaments include not only the neurofilament triplet proteins but also α-internexin and peripherin. Both α-internexin and peripherin are expressed in the neurons of CNS and PNS during development. In adult, peripherin is found abundantly in the neurons of peripheral nervous system, and α-internexin is present mainly in the neurons of central nervous system. We employ neuronal intermediate filaments as probes into developing central neural glands of mouse.
Results from the immunohistochemistry and Western blot indicated that, not only pineal but also posterior lobe of pituitary, both α-internexin and peripherin were start constants expression at P21 and the neuronal triplets proteins were steady display at P90 for pineal gland and at P30 for neurohypophysis. α-internexin and peripherin are colocalized in the perikarya of some cells in the different age of mouse pineal gland. In aged (P360) mouse pineal gland, the expression of neuronal intermediate filaments is augmented as compare with that of the other adult stages. Results from the in situ hybridization and RT-PCR, showed that the number of the mRNA labeling cells of α-internexin and/or peripherin at P7 were the most numerous among all the age stages in mouse pineal. Taken all data together, we concluded that α-internexin-mRNA positive cells are generally more numerous than peripherin-mRNA positive cells during development, and therefore, we suggested that α-internexin-mRNA positive cells were more widely spread than peripherin-mRNA positive cells in pineal gland. In the neurohypophysis, by the in situ hybridization, the mRNAs of α-internexin and peripherin were unexpectedly found in the pituicytes. α-Internexin and NFM mRNAs were also detected in neurohypophysis of developing mouse by mean of RT-PCR. More studies are needed to elucidate the neuronal nature of these specialized glial cells, pituicytes in the neurohypophysis.
In summary, neurohypophysis is earlier than epiphysis not only in start developing time but also in mature period. The phenomenon may cause by more variety and complexity of pineal gland than posterior lobe of pituitary. That needs more investigation about both central glands existing peripherin.
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Carvalho, Cátia Filipa Vieira de. "Dissecting the Role of Caenorhabditis elegans Dynein Light Intermediate Chain in Neuronal Trafficking." Dissertação, 2018. https://hdl.handle.net/10216/118815.
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Carvalho, Cátia Filipa Vieira de. "Dissecting the Role of Caenorhabditis elegans Dynein Light Intermediate Chain in Neuronal Trafficking." Master's thesis, 2018. https://hdl.handle.net/10216/118815.
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CHANG, YEN, and 張妍. "The effects of an intermediate filament protein IFB-1 on mitochondrial transport in C. elegans amphid neurons." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/20869852752738862051.
Full textAbstract:
碩士<br>國立清華大學<br>分子與細胞生物研究所<br>100<br>Mitochondria are essential for survival of eukaryotic cells since they are responsible for ATP synthesis, calcium buffering and apoptosis. Thus, specialized transport and anchoring mechanisms are necessary to distribute and position mitochondria in response to local needs for ATP and calcium buffering. Mitochondrial transport and positioning are particularly challenging in neurons because of the unique geometry and metabolic needs of neurons. In neurons, mitochondria are transported from the soma, where mitochondria biogenesis takes place, to ATP-demanding sites as synaptic terminals and growth cones. Mitochondria remain at these sites until they are transported back to the soma for recycling or degradation. This long-range bidirectional transport mainly depends on microtubules and microtubule-based motor proteins as kinesins and dynein, while short-range mitochondrial transport and docking mainly rely on actin and actin-based motors myosins. In contrast to actin and microtubules, intermediate filaments (IFs) do not possess polarity or associated motor proteins. Therefore, how IFs take part in mitochondrial positioning is relatively unclear. Previous studies suggest that IFs may serve as docking sites for mitochondria, or affect mitochondrial transport through microtubule-based motors.
In this study, we investigate the functions of IFB-1, a C. elegans IF protein, in the mitochondrial transport system of C. elegans amphid neurons. Amphids are sensory organs consisting of a pair of sensilla running along the lateral sides of the worm head. We established wild-type and ifb-1 mutant worms carrying fluorescently-labeled mitochondria in the amphid neurons, and recorded time-lapse images from these worms and their isolated neuronal cells. We found that mutations of IFB-1 lead to larger pools of stationary mitochondria, suggesting a role of IFB-1 in the balance of stationary phases and motile phases of mitochondrial transport. In addition, loss of one isoform of IFB-1 reduces mitochondrial transport velocities and frequencies of changes of directions, but increases pausing frequencies as well as moving persistencies. To explain these complex effects of IFB-1 on mitochondrial motility, we propose a model in which IFB-1 influences mitochondrial transport through affecting kinesin or kinesin-associated proteins.
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Lee, Ting-Hein, and 李亭輝. "The expression of neuronal intermediate filament proteins in the developing mouse olfactory epithelium and olfactory bulb." Thesis, 1998. http://ndltd.ncl.edu.tw/handle/90410238719307512234.
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MacDonald, Stephen Christopher. "Serotonin and noradrenaline modulate excitatory amino acid-evoked currents in acutely isolated intermediate laminae neurons from the neonatal rat spinal cord." 1996. http://hdl.handle.net/1993/19213.
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Johnson-Kerner, Bethany. "Role of Gigaxonin in the Regulation of Intermediate Filaments: a Study Using Giant Axonal Neuropathy Patient-Derived Induced Pluripotent Stem Cell-Motor Neurons." Thesis, 2013. https://doi.org/10.7916/D8Z324C3.
Full textAbstract:
Patients with giant axonal neuropathy (GAN) exhibit loss of motor and sensory function and typically live for less than 30 years. GAN is caused by autosomal recessive mutations leading to low levels of gigaxonin, a ubiquitously-expressed cytoplasmic protein whose cellular roles are poorly understood. GAN pathology is characterized by aggregates of intermediate filaments (IFs) in multiple tissues. Disorganization of the neuronal intermediate filament (nIF) network is a feature of several neurodegenerative disorders, including amyotrophic lateral sclerosis, Parkinson's disease and axonal Charcot-Marie-Tooth disease. In GAN such changes are often striking: peripheral nerve biopsies show enlarged axons with accumulations of neurofilaments; so called "giant axons." Interestingly, IFs also accumulate in other cell types in patients. These include desmin in muscle fibers, GFAP (glial fibrillary acidic protein) in astrocytes, and vimentin in multiple cell types including primary cultures of biopsied fibroblasts. These findings suggest that gigaxonin may be a master regulator of IFs, and understanding its function(s) could shed light on GAN as well as the numerous other diseases in which IFs accumulate. However, an interaction between gigaxonin and IFs has not been detected and how IF accumulation is triggered in the absence of functional gigaxonin has not been determined. To address these questions I undertook a proteomic screen to identify the normal binding partners of gigaxonin. Prominent among them were several classes of IFs, including the neurofilament subunits whose accumulation leads to the axonal swellings for which GAN is named. Strikingly, human motor neurons (MNs) differentiated from GAN iPSCs recapitulate this key phenotype. Accumulation of nIFs can be rescued by reintroduction of gigaxonin, by viral delivery or genetic correction. GAN iPS-MNs do not display survival vulnerability in the presence of trophic factors, but do display increased cell death in the presence of oxidative stress. Preliminary experiments suggest that in iPS-MNs nIFs are degraded by contributions from both the proteasome and lysosome. Gigaxonin interacts with the autophagy protein p62 which has been implicated in the clearance of ubiquitin aggregates by the lysosome, and this interaction is greatly enhanced in conditions of oxidative stress. My data provide the first direct link between gigaxonin loss and IF aggregation, and suggest that gigaxonin may be a substrate adaptor for the degradation of IFs by autophagy, pointing to future approaches for reversing the phenotype in human patients.
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Martins, Rui Pedro Sobral. "Simplificação de modelos através do uso de Data Mining : aplicação à área de medicina intensiva." Master's thesis, 2006. http://hdl.handle.net/1822/26364.
Full textAbstract:
Dissertação de mestrado em Sistemas de Informação<br>O percurso que as ciências médicas têm efectuado nos últimos 30 anos está
estreitamente vinculado ao desenvolvimento tecnológico. A evolução,
aperfeiçoamento e mesmo o despontar de novas técnicas de Inteligência
Artificial (IA) funcionam como impulsionador vital para a criação de novos
métodos de investigação aplicada às mais variadas áreas da medicina.
Pelas suas características muito próprias, quer a nível da constituição das
equipas de intervenção (médicos, enfermeiros e auxiliares) quer pela
vanguarda tecnológica, as Unidades de Cuidados Intensivos (UCI) são locais
perfeitos para a implementação e realização de estudos com vista à
implementação de novos modelos e métodos de investigação.
O presente trabalho pretende apresentar um método complementar ou
alternativo ao actual modelo Simplified Acute Physiology Score (SAPSII) para
determinação do índice de gravidade hospitalar em doentes de UCI baseado
em Eventos Clínicos Adversos (ECA). Por último, os modelos gerados foram
confrontados e analisados recorrendo a técnicas de clustering e
reamonstragem (resampling), constatando–se que os modelos gerados
poderão servir de suporte alternativo para a determinação dos índices de
gravidade hospitalar.<br>Technological developments in the recent years are the most responsible for
the actual clinical medicine course. The fields of Artificial Intelligence,
Knowledge Discovery and Data Mining contributed with innovative and
promising methods and techniques to different domains of medicine, opening
new and exciting opportunities.
Due to its very characteristics, the Intensive Medicine in general, and the
Intensive Care Units in particular, represent an interesting area of application
where the refereed approaches can help and improve the efficiency of the
physicians and the nursing staff.
The existence of huge databases containing information about thousands of
patients and the existence of monitoring equipment, that enables the data
acquisition in real-time, motivated this work.
Nowadays, the severity scores in use, like the SAPS II, encompass some
limitations in its predictive relevance, the time needed to its evaluation and the
costs associated.
Some recent studies postulated the possibility of, alternatively, using the events
and critical events, combined with some personal information, to predict the
patient outcome.
The main goal of this work was to conduct an experimental application of Data
Mining techniques to induce predictive models to complement and simplify the
existing ones. Furthermore, clustering and classification tasks was been
employed in order to small models.
Although at a lower level as expected, the results proved the validity of the
approach.