Dissertations / Theses: 'Neuronal cells'

1

Stanke, Jennifer J. "Beyond Neuronal Replacement: Embryonic Retinal Cells Protect Mature Retinal Neurons." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250820277.

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2

Wang, Li. "CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1184254319.

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3

Anderson, Alexandra Antoinette. "The morphoregulatory function of acetylcholinesterase in neuronal and non-neuronal cells." Thesis, Imperial College London, 2007. http://hdl.handle.net/10044/1/7169.

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4

Doszyn, Olga. "Sex differences in neuronal differentiation of human stem cells." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-384661.

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Sexual dimorphism has been long noted in human neurobiology, apparent most notably in sex-biased distribution of multiple neurological disorders or diseases, from autism spectrum disorder to Parkinson's disease. With the advances in molecular biology, genetics and epigenetics have come into focus as key players in sexually dimorphic neural development; and yet, many studies in the field of neuroscience overlook the importance of sex for the human brain. For this project, human embryonic and neural stem cells were chosen for three main reasons. Firstly, they provide an easily obtainable, scalable and physiologically native model for the early stages of development. Secondly, neural stem cells populations are retained within the adult human brain, and are implicated to play a role in cognition and mental illness, and as such are of interest in themselves. Thirdly, stem cell lines are widely used in research, including clinical trials of transplantation treatments, and for this reason should be meticulously examined and characterized. Here, the morphology, behaviour, and expression of selected genes in four stem cell lines, two of female and two of male origin, was examined in side-by-side comparisons prior to and during neuronal differentiation using a variety of methods including light microscopy, time-lapse two-photon microscopy, quantitative real-time PCR and immunocytochemistry. The obtained results have shown previously uncharacterised differences between those cell lines, such as a higher rate of proliferation but a slower rate of neuronal differentiation in male cell cultures compared to female cells cultivated in the same conditions, and a sex-biased expression of several markers of neuronal maturation at late stages of differentiation, as well as diverse patterns of expression of X- and Y-linked genes involved in stem cell proliferation and neural development.

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Gaughwin, Philip Michael. "Neuronal potential of oligodendrocyte precursor cells." Thesis, University of Cambridge, 2005. https://www.repository.cam.ac.uk/handle/1810/251963.

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6

Heitz, Stéphane Bailly Yannick Kapfhammer Josef P. Poulain Bernard. "Neuronal death mechanisms in cerebellar Purkinje cells." Strasbourg : Université Louis Pasteur, 2008. http://eprints-scd-ulp.u-strasbg.fr:8080/1012/01/HEITZ_Stephane_2008.pdf.

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Thèse de doctorat : Neurosciences : Strasbourg 1 : 2008. Thèse de doctorat : Neurosciences : Universität Basel, Switzerland : 2008.
Thèse soutenue en co-tutelle. Titre provenant de l'écran-titre. Bibliogr. 37 p.

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7

Mark, Melanie Danelle. "The mechanisms underlying EGF-stimulated neuronal differentiation in PC12 cells /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6261.

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8

Perruisseau-Carrier, Claire. "Neuronal commitment of Umbilical Cord Mesenchymal Stem Cells for brain regenerative medicine." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10192.

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De nos jours, aucune prévention ou aucun remède efficace n'existe pour guérir les maladies du cerveau humain. Les cellules souches représentent un grand espoir pour la réparation et la régénération des tissus neuraux endommagés. L'objectif de cette thèse est d'évaluer la capacité des cellules souches du cordon ombilical humain (hUC MSCs) à se différencier en neurones, pour une thérapie cellulaire appliquée au cerveau. Nous avons isolé, multiplié et caractérisé les hUC MSCs naïves à l'échelle des gènes et des protéines. Ensuite, les e_ets sur l'expansion des hUC MSCs et leur différenciation neuronale de différents paramètres ont été évalués par qPCR et marquages immunologiques principalement: milieux et matrices de culture, oxygénation, culture en 3D, ainsi que divers facteurs et molécules tels que les microARNs. Les résultats montrent que les hUC MSCs prolifèrent mieux sans sérum et en conditions de normoxie du cerveau (1-5 % O2). Les hUC MSCs naïves semblent préparées à devenir des neurones à l'échelle des gènes et des protéines, mais pas suffisamment pour supporter leur complète différenciation. L'introduction de microARNs requiert des améliorations pour réguler efficacement les voies de signalisation des hUC MSCs. Au cours de cette étude, nous avons identifé les paramètres favorisant l'expansion des hUC MSCs dans des conditions compatibles avec la clinique. Cependant, une question reste ouverte: les hUC MSCs sont-elles capables de vraie transdifferentiation en neurones fonctionnels malgré les controverses? Des recherches supplémentaires sont nécessaires, mais cette étude constitue une première étape vers l'utilisation des hUC MSCs en médecine régénératrice du cerveau
Nowadays, no effective prevention or cure of human brain diseases is available. Stem cells hold great promise for the repair and regeneration of damaged neural tissues. This thesis aims to evaluate the potency of human umbilical cord mesenchymal stem cells (hUC MSCs) to be committed to the neuronal lineage, for brain cell-based therapy. To achieve this goal, naive hUC MSCs were isolated, expanded, and characterized at the gene and protein level, while particularly focusing on the neuronal lineage and clinical-grade culture conditions. Then, several parameters were investigated for hUC MSCs proliferation and neuronal commitment, including media, coatings, 3D culture, hypoxia, chemicals and molecules. Growth curves drawings, qPCRs, and immunostainings were used among other methods for identifying the best conditions for hUC MSCs expansion, differentiation, culture in 3D, and microRNAs delivery. The results indicate that hUC MSCs better proliferate in serum-free media and brain's normoxia condition (1-5 % O2). Naive hUC MSCs appear primed for neuronal fate at gene and protein level, but not su_ciently to support their neuronal di_erentiation. microRNAs delivery requires further improvement to efficiently promote neuronal signaling pathways in hUC MSCs. Along this study we identified the best parameters for hUC MSCs expansion in clinical-grade conditions. However, a question still remains: are hUC MSCs capable of full transdifferentiation towards functional neurons despite all controversies? Additional work is needed, but this study is a first step towards answering this question, bringing more clues to make transplantation of hUC MSCs for brain regenerative medicine closer

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9

Vogt, Angela Katrin. "Synaptic connectivity in micropatterned networks of neuronal cells." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968908543.

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10

Sridhar, Srikala. "Molecular regulation of neuronal apoptosis in PC12 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq22018.pdf.

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11

Althini, Susanna. "Experimental Studies of BMP Signalling in Neuronal Cells." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3398.

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12

Chawla, S. "Mechanisms controlling calcium-activated transcription in neuronal cells." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597511.

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This thesis describes the finding that changes in calcium concentration in different cellular compartments, the cytoplasm and the nucleus, activate transcription through different DNA regulatory elements in the promoter of the c-fos gene. Transcriptional activation following increases in nuclear calcium concentrations is mediated by the cAMP response element (CRE). A second signalling pathway activates transcription through the serum response element (SRE), is triggered by increases in cytoplasmic calcium and does not require an increase in nuclear calcium. I have also shown that c-fos transcriptional induction mediated through the SRE, is independent of ternary complex formation in AtT20 cells and primary hippocampal neurons. To further characterise nuclear calcium-dependent transcription of c-fos, I identified the transcription factors and coactivators. I showed that the CRE binding protein CREB can mediate a nuclear calcium-dependent response. It is well established that transcriptional activation by CREB requires its phosphorylation on serine 133. This phosphorylation event can occur independently of nuclear calcium transients, indicating that other regulatory steps are necessary for nuclear calcium dependent transcription. These may involve the CREB binding protein CBP. Recruitment of CBP by CREB phosphorylated on serine 133 is critical for CREB-mediated transcriptional responses, raising the possibility that a post-translational modification of CBP may represent a crucial regulatory step in calcium induced transcription. I have shown that the CBP protein when directly tethered to the promoter can confer calcium inducibility to a c-fos based reporter gene and CBP-mediated transcriptional activation requires nuclear calcium transients.

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13

Sawatzky, Deborah Anne. "The interaction of eosinophils with cholinergic neuronal cells." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250421.

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14

Chen, Ya. "Expression of Neuronal Proteins in a Differentiating Human Neuroblastoma Cell Line (IMR32): Insights into Neuronal Development and Disease." online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1133537491.

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15

Matsuda, Akihiro. "(24S)-Hydroxycholesterol efflux from neuronal cells by ABC proteins." Kyoto University, 2014. http://hdl.handle.net/2433/185211.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第17986号
農博第2033号
新制||農||1019(附属図書館)
学位論文||H26||N4811(農学部図書室)
80830
京都大学大学院農学研究科応用生命科学専攻
(主査)教授植田和光, 教授植田充美, 教授三芳秀人
学位規則第4条第1項該当

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16

Leigh, Philippa Jane. "Desensitisation of prostacyclin receptors on neuronal somatic hybrid cells." Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37758.

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17

Baseer, Najma. "Spinal cord neuronal circuitry involving dorsal horn projection cells." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5596/.

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The spinal cord dorsal horn is involved in the processing and transmission of sensory information to the brain. There are several distinct populations of dorsal horn projection cells that constitute the major output of the spinal cord. These cells are mostly found in lamina I and are scattered throughout the deep dorsal horn. There is a population of large lamina III projection cells that expresses the neurokinin 1 receptor (NK1r), which is the main target for substance P released by nociceptive primary afferents. These cells are densely innervated by peptidergic nociceptive afferents and more sparsely by low-threshold myelinated afferents. In addition, they also receive selective innervation from neuropeptide Y-containing inhibitory interneurons. However, not much is known about their input from glutamatergic spinal neurons. It has already been reported that the great majority of large lamina III NK1r expressing cells project to caudal ventrolateral medulla (CVLM) therefore in this study these cells were easily identified without retrograde tracer injection. Preliminary observations showed that these cells received contacts from preprodynorphin (PPD)-containing excitatory axons. The first part of the study tested the hypothesis that lamina III projection cells are selectively targeted by PPD-containing excitatory spinal neurons. Spinal cord sections from lumbar segments of the rat underwent immunocytochemical processing including combined confocal and electron microscopy to look for the presence of synapses at the sites of contact. The results showed that lamina III NK1r cells received numerous contacts from non-primary boutons that expressed vesicular glutamate transporter 2 (VGLUT2), and formed asymmetrical synapses on their dendrites and cell bodies. These synapses were significantly smaller than those formed by peptidergic afferents but provided a substantial proportion of the glutamatergic input to lamina III NK1r projection cells. Furthermore, it was observed that PPD was found to be present in ~58% of the VGLUT2 boutons that contacted these cells while a considerably smaller proportion of (5-7%) VGLUT2 boutons in laminae I-IV expressed PPD. These results indicate a highly selective targeting of the lamina III projection neurons by glutamatergic neurons that express PPD. Fine myelinated (Aδ) nociceptors are responsible for the perception of fast, well-localised pain. Very little is known about their postsynaptic targets in the spinal cord, and therefore about their roles in the neuronal circuits that process nociceptive information. In the second part of the study, Fluorogold injections were made into the lateral parabrachial region (LPb) of the rat brain on one side and cholera toxin B subunit (CTb) was injected into the sciatic nerve on the contralateral side to assess whether Aδ nociceptors provide input to lamina I projection cells. The vast majority of lamina I projection neurons belong to the spinoparabrachial tract, and these can be divided into two major groups: those that express NK1r, and those that do not. The results suggested that CTb labelled a distinct set of Aδ nociceptors, most of which lack neuropeptides. CTb-labelled Aδ afferents formed contacts on 43% of the spinoparabrachial lamina I neurons that lacked the NK1r, but on a significantly smaller proportion (26%) of NK1r projection cells. Combined confocal and electron microscopy established that the contacts were associated with synapses. Furthermore, the contact density of CTb labelled boutons was considerably higher on the NK1r- cells than on those with the NK1r. These results provide further evidence that primary afferents input to projection cells is organized in a specialized way and that both NK1r+ and NK1r- lamina I projection neurons are directly innervated by Aδ nociceptors, thus may have an important role in the perception of fast pain. Lamina I of the rat spinal cord dorsal horn contains a population of large spinoparabrachial projection neurons (giant cells) that receive numerous synapses from both excitatory (VGLUT2) and inhibitory (VGAT) interneurons. The giant cells are selectively innervated by GABAergic axons that express neuronal-nitric oxide synthase (nNOS) and are thought to originate from local inhibitory interneurons. In the rat, the nNOS inhibitory cells belong to a distinct functional population that differs from other inhibitory interneurons in terms of somatostatin receptor (sst2A) expression and also in responsiveness to painful stimuli. There is a population of inhibitory interneurons that express green fluorescent protein (GFP) in lamina II of mice in which GFP is under control of the prion promoter (PrP) and the great majority of these cells also express nNOS. In this part of the study, the inhibitory synaptic input from nNOS-containing GFP boutons to giant lamina I cells was investigated. The great majority of lamina I projection neurons express NK1 receptor; therefore, the possibility that lamina I NK1r-expressing projection neurons received innervation from GFP+/nNOS+ axons was also tested. Since retrograde tracing technique was not used in this part of the study, lamina I projection cells were identified based on the observations made in the previous studies in the rat. Lamina I giant cells were recognized with antibodies against glycine receptor associated protein gephyrin as well as VGLUT2 and VGAT boutons, all of which provide dense innervation to these cells while only those lamina I NK1cells were included in the sample that were large and strongly immunoreactive for NK1r. The results indicated that although GFP axons accounted for only 7-9% of the GABAergic boutons in superficial dorsal horn, they provided over 70% of the inhibitory synapses on most of the giant cells in the PrP-GFP mouse and the great majority of these boutons also contained nNOS. Moreover, a subset of large lamina I NK1r-expressing cells (18/60) received a substantial inhibitory input (> 30%) from GFP+ boutons while the majority of these neurons showed sparse (< 15%) synaptic input. Recently, it has been reported that loss of some inhibitory interneurons in mice lacking the transcription factor Bhlhb5 results in exaggerated itch, and the cells that are lost include many of those that would normally express nNOS. Therefore, in the final set of experiments was designed to test whether there is a reduction in the inhibitory synaptic input to the giant cells in Bhlhb5-/- mouse. Spinal cord sections from Bhlhb5-/- mice and the wild type littermates were processed and analysed to determine any difference in the inhibitory nNOS input to lamina I giant cells belonging to either group. The giant cells from the knockout mice showed a substantial reduction (~80%) in their inhibitory nNOS input; with a moderate reduction in their overall GABAergic input (~35%). There was a considerable increase in nNOS-/VGAT+ boutons in the Bhlhb5-/- mouse (18 ± 4.6 and 37.7 ± 8.2/100 µm of the dendrite in WT and KO, respectively), suggesting some compensation from other nNOS-negative inhibitory interneurons. These results suggest that the loss of nNOS-containing inhibitory synaptic input to lamina I projection cells may contribute to the abnormal scratching behaviour seen in the Bhlhb5-/- mouse. This raises the possibility that the giant cells and a subset of large lamina I NK1r-expressing cells are involved in perception of itch.

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18

Freeman, Caroline Lelia. "The Hereditary Spastic Paraplegia protein strumpellin and the WASH complex in neuronal and non-neuronal cells." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610660.

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Cuddon, Paul. "The role of Ca²⁺ influx in neuronal cell growth and function : a study of hippocampal neurons and neurosphere-derived cells." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615262.

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20

Chatzi, Christina. "Derivation, maintenance and neuronal differentiation of mouse embryonic stem cells." Thesis, University of Aberdeen, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446228.

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This thesis describes successful derivation of 10 novel ES cell lines from C57BL/6J blastocysts. They grow in colonies, express four stem cell markers, display normal karyotype, are able to differentiate in vitro and form chimeras in vivo. Confirmation of germline transmission will enable them to be used for the production of novel mutants on pure C57BL/6J genetic background without backcrossing. The maintenance of stemness of ES cells depends on delicate signalling networks. Spontaneous differentiation is common in ES cell propagation, while its causing factors are largely unknown. The data in this thesis show that ßDC, a dominant negative form of the retinoic acid receptor beta 2, regulates RA-mediated ES cell growth and differentiation. ES cells expressing ßDC are resistant to 100nM RA-induced differentiation in monolayer, while upon 1mM RA induction during aggregation, they differentiate into mesodermal derivatives instead of ectodermal cells. Remarkably, their capacity to participate in normal embryogenesis is not altered by ßDC expression and RA selection. These findings raise the possibility that such a mutant may facilitate long-term maintenance of ES cells. Defective GABAergic signalling is implicated in neurodevelopmental disorders, and brain/spinal cord injuries. As a part of this thesis, a simple differentiation protocol has been developed, which leads to the production of a homogeneous population (93~96%) of GABAergic progenitors from mouse ES cells. Translation of the above technologies to human ES cells may advance the stem cell replacement therapy.

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21

Yu, Chung Ho. "Effects of melia toosendan on neuronal differentiation of PC12 cells /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BICH%202002%20YU.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2002.
Includes bibliographical references (leaves 137-165). Also available in electronic version. Access restricted to campus users.

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22

van, den Bruck David. "Spatial omics in neuronal cells - what goes where and why?" Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20232.

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Intrazelluläre Protein- und RNA-Lokalisation ist ein lebenswichtiger molekularer Mechanismus. Ihm unterliegen sowohl die äußere Gestaltung der Zellform, Zellagilität, zelluläre Differenzierung sowie die intra- sowie interzelluläre Kommunikation. Diverse Krankheiten werden mit Fehlfunktionen des intrazellulären Molekültransportes assoziiert und es existieren unzählige Beispiele für bekannte Wege des intrazellulären Protein- und RNA-Transportes. Allerdings ist die globale Komposition lokaler Protein- und RNA-Reservoirs bisher kaum wissenschaftlich erforscht worden. In dieser Studie beschreibe ich die Protein- sowie RNA-Kompositionen subzellulärer Fraktionen zweier neuronaler Zelltypen. Die Neuriten und Somata von Neuroblastoma-Zellen (N1E-115) und Ascl1 induzierten Neuronen (beides Mauszellen) wurden mechanisch voneinander separiert und mittels RNA-Sequenzierung und Massenspektrometrie auf ihre Bestandteile untersucht. Die Verteilung von mRNAs korreliert signifikant mit der Verteilung der entsprechenden Proteine in Ascl1-iNs während in der Neuroblastoma Zelllinie N1E-115 kein solcher Trend nachgewiesen werden konnte. Der Vergleich zu Datensätzen von anderen Zellsystemen und Methoden zeigt, dass das lokale Proteom sowie das lokale Transkriptome und Translatome stark Zelltyp spezifisch ist. Um den Einfluss lokaler Proteinbiosynthese auf die Komposition subzellulärer Proteinpools zu erheben, habe ich die Lokalisation neu synthetisierter Proteine untersucht. Es scheint, als sei die RNA-Lokalisation und lokale Translation von hoher Relevanz für die Protein-Lokalisation in diesen stark polarisierten Zellsystemen. Des Weiteren stelle ich eine Methode vor, um de novo „zip codes“ in diesen neuronalen Zellsystemen zu identifizieren. Diese könnte ein elementar wichtiger Schritt sein, um Fehlfunktionen im interzellulären Molekültransport zu verstehen.
Intracellular protein and RNA localization is one of the mayor players in the formation of cell shape, enabling cell agility, cellular differentiation and cell signaling. Various diseases are associated with malfunctions of intracellular molecule transport. There are many known pathways of how and why proteins and RNAs are transported within the cell and where they are located, though there is not much known about the global distribution of proteins and RNAs within the cell. In this study I apply a subcellular fractionation method coupled to multiple omics approaches to investigate the global distribution of mRNAs, noncoding RNAs and proteins in neuronal cells. Neurites and soma from mouse neuroblastoma cells (N1E-115) as well as from Ascl1 induced neurons (Ascl1-iNs) were isolated and the composition of the spatial proteome and transcriptome was examined. The localization of mRNAs correlates significantly with the localization of their corresponding protein products in Ascl1-iNs whereas it does not in the mouse neuroblastoma cell line N1E-115. Comparing these datasets with recently published data of other cell lines and methods it is clear, that the local proteome, transcriptome and translatome of neuronal cells is highly cell type specific. To investigate how spatial protein pools are established I analyzed local pools of newly synthesized proteins revealing that many proteins are synthesized on the spot. RNA localization therefore plays a crucial role in generating local protein pools in these highly polarized cell systems. Additionally, I propose a method to identify on a global scale de novo “zip codes” in these cell systems which would be a great step towards understanding malfunctions in molecule transport.

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Brown, Jack. "α7 Nicotinic acetylcholine receptor-mediated calcium signalling in neuronal cells." Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.636524.

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α7 nicotinic acetylcholine receptors (nAChR) are highly permeable to Ca2+ and are clinical targets for Alzheimer’s disease and schizophrenia. The aim of this work was to examine α7 nAChR-mediated Ca2+ signalling in neuronal cells using three different methods, and to evaluate the effects of the desensitizing agonist and prototypical smoking-cessation drug sazetidine-A on α7 nAChRs. Initial studies used 96-well plate assays with SH-SY5Y cells to characterize responses evoked by the α7 nAChR-selective agonist PNU-282987 and positive allosteric modulator PNU-120596. This was complemented by live-imaging of cortical cultures, where the compounds evoked robust Ca2+ responses from 12 % of cells. Co- application with Cd2+, ryanodine and xestospongin-C significantly inhibited these responses, suggesting the involvement of voltage-gated Ca2+ channels and Ca2+- induced Ca2+-release. CNQX and MK801 also significantly inhibited α7 nAChR mediated Ca2+ elevations, indicating a role for glutamate release. A high-content screening assay was developed to further examine these phenomena. Exploratory experiments using KCl, AMPA and NMDA validated a protocol that could be used to image Ca2+ elevations in large cell populations. Inconsistent responses to PNU-120596 and PNU2-282987 were also observed, reflecting the scarcity of α7 nAChRs in cortical cultures and the need for assay optimization. Combination with immunofluorescent labelling revealed α7 nAChR mediated Ca2+ elevations in a subpopulation of astrocytes and neurons, some of which were GABAergic. PNU-120596 potentiated the effects of sazetidine-A in SH-SY5Y cells (EC50 0.4 μM) eliciting responses in 14 % of cells in cortical cultures in a methyllycaconitine- sensitive manner, consistent with α7 nAChR activation. Pre-incubation with sazetidine-A concentration-dependently attenuated subsequent α7 nAChR-mediated responses in SH-SY5Y cells (IC50 476 nM) and cortical cultures, suggesting that α7 nAChRs could play a role in the behavioural effects of sazetidine-A. These comparative experiments enhance our understanding of α7 nAChR signalling and provide a new method to study them further.

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Srinath, Chetan. "mRNA stability in soma and neurites of cultured neuronal cells." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/111314.

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Thesis: S.M., Massachusetts Institute of Technology, Department of Biology, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 45-50).
Neurons rely on mRNA localization and local protein synthesis in neurites to regulate synaptic plasticity, axonogenesis and neural signaling. The local regulation of mRNA stability in neurites is poorly understood. To determine mRNA decay rates, we analyzed the subcellular transcriptomes of neural projections and soma of mouse neuronal cells following inhibition of transcription with actinomycin-D. Less stable transcripts were enriched for GU-rich elements in their 3' UTRs. Around 12% of alternative splicing isoform pairs differed in stability, and cassette alternative ("skipped") exons that negatively impact stability are enriched for A-rich sequences. Overall, decay rates were similar across soma and neurites. However, differences in stability between soma and neurites were observed for GC-rich alternative first exon isoforms, which were preferentially stabilized in neurites. Our results suggest that 5' UTRs may play a key role in regulating local mRNA stability in neurites.
by Chetan Srinath.
S.M.

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25

Li, Ka Wai. "Neuroprotective roles of cefriaxone on cultured astrocytes and neuronal cells." HKBU Institutional Repository, 2011. http://repository.hkbu.edu.hk/etd_ra/1277.

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26

Sime, Wondossen. "The diverse role of laminin isoforms in neuronal cells, human mast cells and blood platelets /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-122-7/.

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Song, Juxian, and 宋聚先. "Protective effects of chrysotoxine on Parkinsonian neurotoxins induceddopaminergic neuronal cell death in SH-SY5Y cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47150129.

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Cetinkaya, Cihan. "Control of growth and differentiation of human neuronal and hematopoietic tumour cells via Myc/Max/Mad-network proteins /." Uppsala : Dept. of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, 2005. http://epsilon.slu.se/200522.pdf.

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Sartor, Francesca. "Regulation of translation initiation and RNA decay is important for neuronal differentiation." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=.

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30

Tomba, Caterina. "Primary brain cells in in vitro controlled microenvironments : single cell behaviors for collective functions." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENY039/document.

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Du fait de sa complexité, le fonctionnement du cerveau est exploré par des méthodes très diverses, telles que la neurophysiologie et les neurosciences cognitives, et à des échelles variées, allant de l'observation de l'organe dans son ensemble jusqu'aux molécules impliquées dans les processus biologiques. Ici, nous proposons une étude à l'échelle cellulaire qui s'intéresse à deux briques élémentaires du cerveau : les neurones et les cellules gliales. L'approche choisie est la biophysique, de part les outils utilisés et les questions abordées sous l'angle de la physique. L'originalité de ce travail est d'utiliser des cellules primaires du cerveau dans un souci de proximité avec l'in vivo, au sein de systèmes in vitro dont la structure chimique et physique est contrôlé à l'échelle micrométrique. Utilisant les outils de la microélectronique pour un contrôle robuste des paramètres physico-chimiques de l'environnement cellulaire, ce travail s'intéresse à deux aspects de la biologie du cerveau : la polarisation neuronale, et la sensibilité des cellules gliales aux propriétés mécaniques de leur environnement. A noter que ces deux questions sont étroitement imbriquées lors de la réparation d'une lésion. La première est cruciale pour la directionalité de la transmission de signaux électriques et chimiques et se traduit par une rupture de symétrie dans la morphologie du neurone. La seconde intervient dans les mécanismes de recolonisation des lésions, dont les propriétés mécaniques sont altérées., Les études quantitatives menées au cours de cette thèse portent essentiellement sur la phénoménologie de la croissance de ces deux types de cellules et leur réponse à des contraintes géométriques ou mécaniques. L'objectif in fine est d'élucider quelques mécanismes moléculaires associés aux modifications de la structure cellulaire et donc du cytosquelette. Un des résultats significatifs de ce travail est le contrôle de la polarisation neuronale par le simple contrôle de la morphologie cellulaire. Ce résultat ouvre la possibilité de développer des architectures neuronales contrôlées in vitro à l'échelle de la cellule individuelle
The complex structure of the brain is explored by various methods, such as neurophysiology and cognitive neuroscience. This exploration occurs at different scales, from the observation of this organ as a whole entity to molecules involved in biological processes. Here, we propose a study at the cellular scale that focuses on two building elements of brain: neurons and glial cells. Our approach reachs biophysics field for two main reasons: tools that are used and the physical approach to the issues. The originality of our work is to keep close to the in vivo by using primary brain cells in in vitro systems, where chemical and physical environments are controled at micrometric scale. Microelectronic tools are employed to provide a reliable control of the physical and chemical cellular environment. This work focuses on two aspects of brain cell biology: neuronal polarization and glial cell sensitivity to mechanical properties of their environment. As an example, these two issues are involved in injured brains. The first is crucial for the directionality of the transmission of electrical and chemical signals and is associated to a break of symmetry in neuron morphology. The second occurs in recolonization mechanisms of lesions, whose mechanical properties are impaired. During this thesis, quantitative studies are performed on these two cell types, focusing on their growth and their response to geometrical and mechanical constraints. The final aim is to elucidate some molecular mechanisms underlying changes of the cellular structure, and therefore of the cytoskeleton. A significant outcome of this work is the control of the neuronal polarization by a simple control of cell morphology. This result opens the possibility to develop controlled neural architectures in vitro with a single cell precision

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You, Sijun. "Long-term fate of non-neuronal cells in denervated nerve stumps." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1995. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq22046.pdf.

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Ali, Hamad. "Neuronal potential of umbilical cord blood non-hematopoietic multipotent stem cells." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1277.

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The human central nervous system, one of the most complex organ systems anatomically and physiologically in the human body, is the body control center which manages and coordinates functions of all different organ systems. The lack of effective treatments and therapeutic intervention make injuries and disorders associated with the central nervous system one of the most dangerous and fatal health conditions worldwide. The adult nervous system has a limited capability of self-repair and regeneration following either a neurological disorder or injury. Despite being limited and ineffective in initiating recovery from injuries and disorders, this property opened the doors for a new direction of research aimed at investigating the possibility of developing therapies and treatments for central nervous system injuries and disorders based on the concept of regeneration and cell transplantations. Stem cells have gained significant public attention over the past decade due to their differentiation capabilities and potential utilization in clinical applications. The ability to differentiate stem cells into neural lineages including neurons and glial cells, highlighted their potential role as a therapeutic tool for central nervous system injuries and disorders. The main aim of this thesis is to show that umbilical cord blood stem cells are a potential source of cells that could be used therapeutically in central nervous system injuries and disorders. A distinct population of cells has been purified from human umbilical cord blood. These cells have been characterized and differentiated in-vitro into neuron-like cells using fully defined sequential neuronal induction protocol. The differentiated cells were shown to have similar morphological and functional properties to developing central nervous system endogenous neurons using several different techniques, including immunocytochemistry, real-time PCR, cDNA arrays and calcium imaging. The results highlight the potential role of umbilical cord blood stem cells as a therapeutic tool for central nervous system injuries and disorders for which current mode of therapy is inadequate. In addition, they might provide an in-vitro model of neural cells for toxicology and drugs testing research.

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Adams, Natalie. "Quantifying activity in nascent neuronal networks derived from embryonic stem cells." Thesis, University of Newcastle Upon Tyne, 2013. http://hdl.handle.net/10443/1860.

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The relationship between spatiotemporal patterns of spontaneous activity and functional specialisation in developing neuronal networks is complex and its study is crucial to our understanding of how network communication is initiated. This project quantifies transitions between structural and functional states in embryonic stem cell cultures during differentiation. The work also focussed on the role of γ-aminobutyric acid (GABA), known to be vital for neuronal network development. The work used many techniques, including carbon nanotube (CNT) -patterned substrates to manipulate network architecture, multi-electrode arrays (MEAs) and calcium imaging to quantify function. An embryonic stem cell line (CC9) was used to generate ‘de novo’ neuronal networks and these were monitored over 13 – 22 days in vitro (DIV), while network structure forms and stabilizes. On CNT-patterned arrays, differentiating CC9s migrated and sub-clustered on CNT islands showing that network structure could be manipulated. No spontaneous electrophysiological (unit) activity was found in these cultures. However, intracellular calcium responses were readily induced and seen spontaneously at 13-20 DIV. Activity rate, kinetics and number of active cells increased between 16-18 DIV, correlating with changes in network clustering. Post 17 DIV, activity transformed from near-random to periodic and synchronous. Many events were initiated by ‘hubs’ and degrees of critical behaviour were observed, moving towards more efficient information processing states with development. Blockade of GABAA receptors lead to elevated spontaneous activity and supercritical behaviour, depending on developmental stage. Application of exogenous GABA induced large, slow calcium transients in a developmental stage-dependent manner, suggestive of a mixed excitatory/inhibitory role. These findings begin to show how activity develops as stem cells differentiate to form neuronal networks. GABA’s role in controlling patterns of activity was more complex that previously reported for neuronal networks in situ, but GABA clearly played a vital role in shaping population behaviour to optimise information processing properties in early, developing networks.

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游思維 and Siwei You. "Neuronal survival and axonal regeneration of retinal ganglion cells inadult hamsters." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B3123799X.

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Helwig, Bryan Glen. "Neuronal differentiation of stem cells derived from human umbilical cord matrix /." Search for this dissertation online, 2003. http://wwwlib.umi.com/cr/ksu/main.

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Lawton, Michelle. "The effect of heavy metals on differentiated neuronal and glial cells." Thesis, Nottingham Trent University, 2007. http://irep.ntu.ac.uk/id/eprint/219/.

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Heavy metal poisoning poses a serious health risk among populations worldwide. The symptoms presented by exposure are varied and depend upon the species of the metal, the age of the individual and the exposure dose. All heavy metals have debilitating effects on the CNS. Children are especially sensitive to the neurological effects due to the intense growth and activity of a developing nervous system and inadequately developed defences. The aims of this study were to determine the effects of sub-lethal concentrations of numerous heavy metals on neuronal and glial cell differentiation. Using established cellular models, the toxicity of zinc, lead, mercury, methylmercury and thimerosal were investigated using assays of cell viability and morphology on differentiating N2a and C6 cells. Initial research revealed thimerosal, methylmercury and cadmium to be the most toxic compounds tested, in terms of their ability to inhibit the outgrowth of neurites in both cell lines at sub-lethal concentrations. Although cadmium chloride showed similar patterns of toxicity to the mercury compounds, thimerosal and MeHgCl were chosen for further investigation at a molecular level. Methylmercury chloride a common environmental pollutant and thimerosal; a preservative found in many medicines, were chosen for further investigation, as previous work has demonstrated the health risks posed by the two organic mercury compounds but little is known about non-lethal changes that occur in the nervous system, especially with thimerosal. Both thimerosal and MeHgCl inhibited MTT reduction and neurite outgrowth after 4 and 24 hours exposure at sub-lethal concentrations (0.1 and 1 µM). The inhibition of neurite outgrowth by sub-lethal concentrations of MeHgCl and thimerosal was accompanied by cytoskeletal changes in the cells. At 4 hours in C6 cells there was no change in the levels of tyrosinated a-tubulin, whereas in N2a cells the level of tubulin tyrosination was shown to be reduced compared to the control. Both cell lines exhibited a fall in total a-tubulin, tyrosinated a-tubulin and total ß-tubulin after 24 hours of exposure to organic mercury compounds, indicating proteolysis and/or reduced synthesis of the tubulin subunit. N2a cells also showed a decrease in the levels of phosphorylation in the neurofilament heavy chain after 4 hours of exposure to thimerosal and MeHgCl, whereas after 24 hours there appeared to be proteolytic degradation, as the total neurofilament heavy chain levels were reduced compared to the untreated controls. Reduced levels of tubulin and NFH were confirmed by immunofluorescence staining of fixed cell monolayers. Western blotting analysis also indicated increased ERK activation in glial cells incubated with 0.1 and 1 µM thimerosal for 4 hours, followed by reduced activation after 24 hours exposure, whereas exposure to MeHgCl decreased the levels of ERK activation at both time points. In the neuronal cell line ERK activation was suppressed at both 4 and 24 hours and with both concentrations of the organic mercury compounds. As ERK activation plays a key role in the regulation of neurite outgrowth and NFH phosphorylation, both of which were inhibited by the addition of thimerosal and MeHgCl, the findings are consistent with a role for disrupted ERK signalling in the sub-lethal toxicity of these compounds. Both thimerosal and MeHgCl caused redistribution of SERCA and ryanodine receptors, both of which are mechanisms by which intracellular Ca2+ concentrations are maintained. As the endoplasmic reticulum (ER) houses both SERCA and ryanodine receptors, the reorganisation may indicate that organic mercury compounds cause redistribution of the ER. Such disruption may lead to sustained increases in intracellular Ca2+, causing elevated activity in Ca2+ dependant enzymes. Indeed, western blotting analysis and enzyme assays showed that calpain activity (particularly calpain 1) increased in response to sub-lethal concentrations of the organic mercury compounds. As calpains target cytoskeletal proteins, the increased activity may be at least partly responsible for reduced levels of tubulin and NFH.

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Kelly, B. "Characterisation and functional analysis of protease activated receptors in neuronal cells." Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273045.

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Thwaites, J. W. "Methods affecting neuronal differentiation of human adult and pluripotent stem cells." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1467088/.

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Stem cells have significant potential to treat many age-related degenerative disorders that affect increasing numbers of people globally. This thesis investigated the capacity for omnicytes and human pluripotent stem cells (hPSC) to undergo directed differentiation towards neuronal cell types for the treatment of ischemic stroke and Parkinson’s disease respectively. Omnicytes express a range of markers related to pluripotency and plasticity; however they are a challenging cell source to use in the development of cell therapies. Variability in omnicyte quality was associated with patient source, disease type and cryopreservation, all of which affected the reproducibility of data. Successful generation of dopaminergic neurons was achieved using a suspension-based hPSC culture system, with modified culture medium designed to replicate endogenous signalling during development. Neurons expressing key markers of dopaminergic neurons were generated and were capable of producing dopamine in response to KCl challenge. The work also showed that transfection of saRNA could enhance the expression of key genes i.e. foxa2, lmx1a and TH, relative to mock transfected cultures, although not significantly. Results also showed that the specific hESC line used (Shef6) had a greater propensity for differentiation toward dopaminergic neurons than MSUH001 hiPSC. This work successfully used saRNA to enhance gene expression, but shows that transfection efficiency is a limiting factor to its use. However, if transfection efficiency can be addressed, saRNA will become a powerful tool in the generation of cell therapies, particularly if it can be applied to suspension cell cultures.

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Basavappa, Srisaila. "Hypoosmotically-activated anion permeability in the human neuroblastoma cell line CHP-100." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318761.

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Moore-Dotson, Johnnie M., Jamie J. Beckman, Reece E. Mazade, Mrinalini Hoon, Adam S. Bernstein, Melissa J. Romero-Aleshire, Heddwen L. Brooks, and Erika D. Eggers. "Early Retinal Neuronal Dysfunction in Diabetic Mice: Reduced Light-Evoked Inhibition Increases Rod Pathway Signaling." Association for Research in Vision and Ophthalmology (ARVO), 2016. http://hdl.handle.net/10150/604678.

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Recent studies suggest that the neural retinal response to light is compromised in diabetes. Electroretinogram studies suggest that the dim light retinal rod pathway is especially susceptible to diabetic damage. The purpose of this study was to determine whether diabetes alters rod pathway signaling.

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Lau, See-yan. "A study of intracellular signals of K-opioids in non-neuronal cells /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19667139.

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Wiskow, Ole. "Evaluation of the neuronal differentiation capacity of pluripotent stem cells and neural stem cells in monolayer culture." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609417.

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劉思恩 and See-yan Lau. "A study of intracellular signals of K-opioids in non-neuronal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31214290.

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You, Siwei. "Neuronal survival and axonal regeneration of retinal ganglion cells in adult hamsters /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19859946.

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Yang, Xiu. "ALTERED NEURONAL LINEAGES IN THE FACIAL GANGLIA OF Hoxa2 MUTANT MICE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1207189742.

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Bezuidenhout, Lois-Mary. "Triquinylamines as regulators of calcium homeostasis of neuronal cells / Lois-Mary Bezuidenhout." Thesis, North-West University, 2007. http://hdl.handle.net/10394/1470.

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Römer, Lutz [Verfasser]. "Pro- and antidegenerative effects of JNK stresskinases in neuronal cells / Lutz Römer." Kiel : Universitätsbibliothek Kiel, 2008. http://d-nb.info/1019541253/34.

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Haddley, Kate. "Transcriptional regulation of the preprotachykinin-A (PPT-A) gene in neuronal cells." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408571.

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Contestabile, Andrea <1971&gt. "Regulation of transcription factor Lot1 expression during proliferation/differentiation of neuronal cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/445/.

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Curry, Nathan. "Development and application of correlative STED and AFM to investigate neuronal cells." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/274579.

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Over the past three decades in cellular neuroscience there has been a shift towards the view of the 'tripartite synapse', where, astrocytes -- as well as the pre-synapse and post-synapse -- are involved in synaptic signalling. The migration of astrocytes to form branched networks in the brain is, therefore, of great interest in understanding brain development and neuronal function. Migration is a complex interplay between cytoskeletal reorganisation and cell mechanical stiffness. In order to improve understanding of this process, correlative measurements of cytoskeletal organisation and mechanical stiffness are required. To investigate astrocyte migration a technique combining atomic force microscopy (AFM) with stimulated emission depletion (STED) microscopy was developed. First a custom STED microscope was developed. To facilitate the design of this system the theoretical performance of a range of STED techniques (cw-STED, time-gated STED, pulsed STED and RESOLFT) were compared, identifying that pulsed STED theoretically has the highest photon efficiency. A pulsed STED microscope, which uses adaptive optics, was then designed, developed and characterised. The microscope was found to achieve resolutions below 50 nm. The STED microscope was combined with a commercial AFM to study live cells. Using the recently developed SiR-actin and SiR-tubulin dyes and AFM probes optimised for live cell mechanical property studies, images of the actin and tubulin cytoskeleton were correlated with AFM topography and mechanical stiffness measurements. It was found that, in astrocytes, actin contributes significantly both to astrocyte stiffness and topography. Investigations of migrating cells showed differences in actin organisation and mechanical stiffness between the basis and leading edge of migration. A further study was performed, investigating the effects of the gap-junction protein connexin30, which is expressed during the early stages of brain development, on migration. This protein was found to inhibit the actin reorganisation and mechanical stiffness changes observed in basal conditions. Overall the combination of mechanosensitive AFM measurements with advanced microscopy, such as super-resolution, on live cells is a promising approach which will enable a range of investigations, for instance when studying cell structural remodeling during brain development or tumorigenesis.

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Dissertations / Theses on the topic 'Neuronal cells'

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