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Published: 10 December 2022
Last updated: 28 January 2023

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1

Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.

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2

Roshan, Payam. "Cellular basis of inflammation in the enteric nervous system." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26759.

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There is limited knowledge of immunocyte-myenteric neuronal interaction and the role of iNOS in myenteric neuronal injury. This research sought to examine the role of macrophages, NO, and iNOS inhibitors in myenteric neurodegeneration. Increased NO synthesis in macrophages and its effects on myenteric neurons were investigated in cell cultures. Using rodent models of inflammation, we further examined NO-dependent neurotoxicity. In the presence of activated macrophages neuronal injury and degeneration occurred; however the myenteric neurons showed greater resistance to oxidative challenge than cortical neurons. Pretreatment with iNOS inhibitors significantly reduced these inflammatory effects. Myenteric neuronal injury was also evident in experimental colitis, and iNOS selective inhibitor protected the myenteric neurons from inflammation and degeneration. In conclusion, these results show that activated macrophage-derived NO is important in inflammation-dependent myenteric neurodegeneration, and iNOS inhibitors can protect myenteric neurons from degeneration. Two potential strategies for neuroprotection in gut inflammation are defined.
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3

Ford, Melanie. "Cellular prion protein expression in the mouse." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249698.

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4

Balaskas, Christos. "Cellular development of the enteric nervous system in the chick embryo." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267801.

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5

Bogni, Silvia. "Molecular and cellular analysis of the enteric nervous system in vivo." Thesis, Open University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402166.

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6

Schuldt, Alison Jean. "The generation of cellular diversity in the Drosophila central nervous system." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624291.

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7

WILLIAMS, JON. "EFFECTS OF LOSS OF NF1 GENE ON PERIPHERAL NERVOUS SYSTEM PROGENITORS AND TUMORIGENESIS." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1212181112.

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8

Pliego-Rivero, Francisco Bernardo. "Thy-1 : cellular compartmentalization during development and participation in signal transduction." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358073.

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9

Franceschini, Isabelle A. "Cellular and molecular studies on olfactory bulb ensheathing cells." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301803.

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10

Brownlee, David Joseph Acheson. "Putative neurotransmitters in selected helminth parasites : cellular and subcellular localisation." Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296822.

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11

Cooper, Jason Christian Todd. "Agmatine, Decarboxylated Arginine, is a Transepithelial Signal to the Enteric Nervous System." Thesis, Mississippi College, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10686492.

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Recent advances regarding commensals in the gastrointestinal tract point to an intimate “accessory” organ status. To study the cross-talk that an accessory organ must have, the Piletz laboratory began in 2014 developing a three-dimensional (3D) in vitro co-culture model system, whereby two differentiated cell lines are juxtaposed along with “luminal” contents. The model uses differentiated C2BBe1 cell line enterocytes grown to confluency on polycarbonate filters with 0.4 µm pores over-layered atop SH-SY5Y cell line neurons to study cross-talk from either the lumen-side or the neuron-side. The focus is on an endogenous molecule, agmatine (1-amino-4-guanidobutane), made by gut bacteria at millimolar concentrations in the mucosa of the small intestine—yet in the brain known to be a neurotransmitter. Starting with each individual cell line in standard mono-cultures, agmatine was added at varying doses and varying times to replicate what is essentially dogma to the agmatine field, that of being anti-proliferative to all mammalian cells. Above 1 mM agmatine, the predicted anti-proliferative response was realized as a non-toxic, non-divisional state sustained for at least 4 days from single dosing. Moving to the 3D co-culture system, wherein the C2BBe1 cells were differentiated as per high transepithelial electrical resistance (TEER) over a 24-hour equilibration period, it was expected that agmatine would again be anti-proliferative. Yet, apical agmatine appeared to exert a pro-proliferative effect starting as low as 0.002 mM. A parallel decline in metabolism per SH-SY5Y cell was found using the color dye reaction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). It was therefore hypothesized that apical agmatine had caused the C2BBe1 cells to secrete a growth signal(s) impacting the underlying SH-SY5Y cells; and to test this, conditioned basal media collected from just C2BBe1 cells grown 4 days in the presence of apical 2 mM agmatine was taken to replace the media of naïve SH-SY5Y cells growing in log phase mono-cultures. The expectation was that growth factors would be carried over, but to the contrary, an anti-proliferative response emerged from the conditioned media, mirroring the earlier studies with agmatine in mono-cultures. Cellular lysates were also prepared from treated cells exposed for 24 h to 2 mM agmatine, and these were probed on immune-blots to assess if any of 32 common receptor tyrosine kinases had phosphorylated /activated post-addition of apical mM agmatine. No evidence was obtained that agmatine (mM apical) had elicited such flags of cell activation. Next, the 3D co-culture condition was re-run for longer periods and with more controls, and from this came the realization that the model had hidden the existence of an anti-proliferative response from the C2BBe1 cells before agmatine was even added. In short, the starting hypothesis was disproven, but in doing so it was realized that micromolar apical agmatine is able to rejuvenate a cytostasis rendered by the C2BBe1 co-culturing. Two fundamentally different mechanisms must be invoked by agmatine, because the concentrations of agmatine at which these two processes occurred were 500-fold different (0.002 mM for the reversal of cytostasis vs. 1 mM for anti-proliferative, respectively). In summary, any microbial dysbiosis involving agmatine-producing bacteria is likely to act through two molecular signaling mechanisms from the “accessory” organ bacteria to enteric nervous system.

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12

Etheredge, Jack. "Transcriptional profiling of Drosophila larval ventral nervous system hemilineages." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270548.

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Over 90% of neurons in the adult CNS of Drosophila are born from neuronal stem cells (neuroblasts) during the post-embryonic phase of neurogenesis. Most of the post-embryonic neurons derive from type I neuroblasts, which undergo repeated asymmetric divisions to produce a series of ganglion mother cells (GMCs). Each GMC then divides once resulting in two neurons, the “A” (Notch-on) and “B” (Notch-off) daughters. The respective daughter neurons of each type then constitute the A and B hemilineages for that neuroblast. 33 postembryonic hemilineages contribute neurons to each thoracic hemisegment, and these immature neurons arrest their development at a similar stage until metamorphosis. These arrested neuroblast lineages are uniquely identifiable by morphology. Access to a large pool of clonally-related and morphologically similar neurons makes this system tractable to RNA-seq analysis, since one can genetically label and isolate many cells per animal, which are predicted to share similar gene expression profiles. Our primary focus is to examine hemilineages with similar targets (e.g. leg neuropil) to identify genes that are required to establish and maintain hemilineage identity early in development. Given that activating these hemilineage neurons as a group drives distinct behaviors and that they form morphologically coherent structural units during development, we hypothesized that these hemilineages should express patterns of genes that are: 1) distinct from other hemilineages and 2) characteristic of individual hemilineages. We have used hemilineage-specific GAL4 lines to isolate hemilineages for RNA-seq analysis, ultimately gathering data for 11 of the 33 hemilineages as well as for some larger populations of neurons. We found that, in addition to combinatorial patterns of genes specifying the hemilineage neurons, there are some genes that are expressed by only a single hemilineage within the ventral nervous system (VNS). Most hemilineages display unique expression of certain transcription factors (TFs) and axon guidance genes. We collected data for two pairs of sibling hemilineages (lineage 1 and lineage 12) in order to identify differences between the A and B hemilineages derived from a common neuroblast. While A neurons display greater overall transcriptional diversity than B neurons, sibling hemilineages share very similar expression profiles. Comparing the gene expression between immature and mature larval neurons revealed that mature neurons express many genes not expressed in immature neurons, such as neuropeptide signaling genes and many neurotransmitter and ion channel genes associated with mature neuron function. Birth order also appears to dictate many differences in expression profile. Late-born immature neurons are typified by a period of transient Notch-related gene expression that is absent from early-born neurons. We are characterizing the function of many differentially expressed genes in particular hemilineages.
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13

Hall, Deborah Jean. "Cytokines and their inhibition within the central nervous system in chronic relasping experimental allergic encephalomyelitis." Thesis, University of York, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238710.

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14

de, Lange Anja. "Exploring molecular and cellular mechanisms underlying seizures in neurocysticercosis." Doctoral thesis, Faculty of Health Sciences, 2021. http://hdl.handle.net/11427/33597.

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Neurocysticercosis is a disease in which larvae of the tapeworm, Taenia solium, infect the central nervous system of humans. Seizures are the most common symptom of NCC, occurring in between 70 % and 90 % of all symptomatic NCC cases. Neurocysticercosis impacts heavily on the quality of life of patients, and further presents a significant drain on the economic resources of endemic countries. Despite its considerable global impact, the molecular and cellular mechanisms underlying seizures in neurocysticercosis remain largely unknown. In this thesis I have explored novel models for neurocysticercosis by combining mouse hippocampal organotypic brain slice cultures with various preparations of a model parasite, Taenia crassiceps. Utilising these models, I first explored, using patch clamp and local field potential electrophysiology, how Taenia larval extracts directly affect neuronal excitability. I report that extracts of Taenia crassiceps resulted in a significant acute excitation of neurons and triggered seizure-like events in brain slices. Further investigation revealed that this excitation was mediated by the activation of glutamate receptors and that, indeed, the larvae of both Taenia crassiceps and Taenia solium contain and produce levels of glutamate sufficient to explain this effect. Chronic exposure of brain slices to intact, living, larvae did not, however, result in any changes in network excitability. Next, I investigate whether Taenia larvae produce acetylcholinesterases, as these enzymes have the potential to affect neuronal signaling by digesting the neurotransmitter acetylcholine. Ellman's assays, in situ acetylcholinesterase activity assays, and patch clamp electrophysiology reveal that both Taenia crassiceps and Taenia solium larvae produce acetylcholinesterases and that the activity of Taenia acetylcholinesterases is sufficient to digest acetylcholine at a concentration that alters neuronal signaling. Finally, I explore the effect that Taenia larval extracts have on the innate immune cells of the brain, as the responses of these cells can also alter neuronal excitability. Through the measurement of brain slice cytokine release using enzyme-linked immunosorbent assays, I discover that Taenia crassiceps extracts have robust antiinflammatory effects, which involve lipid, protein, and glycan elements. This thesis presents novel findings that reveal ways in which Taenia larvae interact with both neuronal and nonneuronal resident brain cells. It further delves into how these interactions could contribute to seizure generation in neurocysticercosis and proposes some potential new therapeutic approaches to treat seizures in neurocysticercosis.
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15

Tam, Chun-yat, and 譚俊逸. "Genetic interaction between Patched1 and Sox10 in enteric nervous system development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/211149.

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The enteric nervous system (ENS) is derived from neural crest cells (NCCs). Once these NCCs reach the foregut, they are recognized as enteric NCCs(ENCCs) which subsequently colonize the gastrointestinal track. The proliferation, migration and neuronal versusglial differentiation of ENCCs are tightly controlled by multiple signaling pathways and transcription factors. Impaired ENS development may result in various human congenital disorders such as Hirschsprung disease(HSCR). Hedgehog (Hh) signaling is a key element in ENS development. Patched-1 (Ptch1) is a negatively regulated receptor for Hh. Binding to Hh or deletion of Ptch1releases its inhibitory function and activates the Hh signaling cascade. Our group has previously revealedPTCH1as a susceptibility gene for HSCR. In particular, NCC-specific deletionofPtch1in mice led to premature glial differentiation and depletion of proliferative ENCC pool, but the molecular mechanisms are still not very clear. Sox10, a member of SRY-related HMG-box family transcription factor, is implicated in these two processes of ENS development. It prompted us to hypothesis that Ptch1 may interact with Sox10 to control ENCC proliferation and glial lineage differentiation. In this study, I generated compound mouse mutants to i) investigate the potential functional interaction between Ptch1 and Sox10 in ENCC differentiation and proliferation, and ii) examine the link between the perturbed NCC differentiation and aberrant proliferation of ENS progenitors, to determine how interruption of these processes may lead to intestinal hypoganglionosis of Ptch1mutants. I found that persistent Hh activation through deletionofPtch1causes a differentiation bias toward glial lineage. Ptch1mutants consistently contained more Sox10expressing glial committed ENCCs and exhibited premature gliogenesis. To test whether elevated Sox10expressing cells contribute in the ENS phenotypes of Ptch1 mutants, 〖Sox10〗^(NGFP/+); Ptch1 compound mutants were generated, where one copy of Sox10 was deleted. Immunohistochemical analysis revealed that 〖Sox10〗^(NGFP/+) mutants exhibitpremature neurogenesis as reported previously, while the proliferation and glial differentiation of ENCCs are not affected.On the other hand, in the compound mutants, heterozygous deletion of Sox10 markedly rescued premature gliogenesis caused by deletion of Ptch1. These data suggest that Ptch1 regulates gliogenesis of ENCCs through maintaining Sox10 expression. To delineate how premature glial differentiation of ENCCs leads to hypoganglionosis, I further investigated whether the differentiation defect perturbs the proliferation capacities of ENCCs. Correction of glial differentiation defect in Ptch1 mutant by heterogeneous deletion of Sox10 could significantly restore the pool size of the proliferative ENCCs of the compound mutant. This observation implies that proliferation defects in Ptch1 mutant represents a secondary consequence of premature gliogenesis, highlighting the close link between these two developmental processes. In summary, the current study provides evidence that Sox10 works coordinately with Ptch1 to mediate ENS development. Loss of Ptch1 favors glial differentiation and formation ofSox10 expressing glial progenitors, leading to intestinal hypoganglionosis as seen in Hirschsprung’s disease.
published_or_final_version
Surgery
Master
Master of Philosophy
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16

Sjöblom, Markus. "The duodenal mucosal bicarbonate secretion : role of melatonin in neurohumoral control and cellular signaling /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. {[distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3521.

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17

Eade, Kevin Thomas. "Subsets of developmental transcription networks maintain cellular subtype identity in the mature nervous system." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/40717.

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The diversification of cellular subtype during development is directed by combinatorially acting transcription factors and signaling pathways that act to regulate subtype specific gene expression profiles in post-mitotic cells. These key transcription factors and signaling pathways operate in a transcriptional network, which act to establish cellular subtype identity over the course of a developing cellular lineage. Lineage progression towards ever increasing cellular diversity is often viewed as a ratchet mechanism of irreversible steps resulting in the specification and then terminal differentiation of cell subtype identities. From this viewpoint, terminally differentiated cells have long been considered as irreversibly locked into their identity. In a landmark article, Blau and Baltimore (Blau and Baltimore, 1991) postulated that a cell’s identity, or differentiated status, requires persistent active regulation, rather than lapsing into a passive ‘locked-in’ state. While little genetic evidence was available at the time, sufficient evidence has since accumulated to propose that the terminally differentiated state, or identity, of a cell subtype indeed requires active maintenance. Currently, however, we have only the most rudimentary understanding of the regulatory mechanisms that maintain neuronal identity. This thesis presents a systematic effort to characterize the role of the transcriptional networks that differentiate neuronal identity in the mature neurons of the adult nervous system. Using the Drosophila Tv cluster neurons I show the persistent requirement of 1) target derived signals and 2) networks of transcription factors for the maintenance of the cellular subtype specific expression profiles of terminal differentiation genes, genes that define these neuron’s function and identity. This work establishes one of the most comprehensive transcriptional models for maintenance of cell identity to date. It also provides novel mechanistic insights showing that cellular differentiation is a persistent process that requires active maintenance, rather than being passively ‘locked-in’ or unalterable. As such, the work of this thesis provides critical insight that provides a strong foundation for further efforts to determine how neuronal identity is maintained.
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18

Rao, Rohit R. "The Microenvironment as a Regulator of Nervous System Development, Brain Tumor Growth and Treatment Resistance." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1624917824334193.

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19

Ooi, Felicia Kye-Lyn. "Uncovering how the nervous system controls the cellular stress response in the metazoan Caenorhabditis elegans." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6236.

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The ability to accurately predict danger and implement appropriate protective responses is critical for survival. Environmental fluctuations can cause damage at the cellular level, leading to the misfolding and aggregation of proteins. Such damage is toxic to cells: in age-related neurodegenerative diseases like ALS, Parkinson’s, Alzheimer’s and Huntington’s Diseases, the accumulation of damaged proteins in the brain ultimately leads to neuronal cell death and disease onset. To date, there is still no cure to combat the progressive degeneration and cell death seen in the brains of patients. Cells within an animal possess defense programs to minimize protein damage. One such defense mechanism is the activation of a program called the Heat Shock Response, which increases production of protective proteins known as heat shock proteins (HSPs). These HSPs act as molecular chaperones to assist with the clearing out of damaged proteins. This program is implemented by a conserved transcription factor, Heat Shock Factor 1 (HSF-1). However, in brains of patients with degenerative diseases, this protective mechanism, for reasons yet unknown, is not constantly activated. My thesis has involved the discovery of innate mechanisms that exist in organisms to activate this cellular protective mechanism against protein misfolding. My research, using the model organism Caenorhabditis elegans, has shown that the protective heat shock response in the cells of the animal can be triggered through neurohormonal signaling. The neurohormonal signaling that I am studying is one that is highly conserved across all organisms from plants to insects to mammals – serotonergic signaling. The stimulation of serotonergic signaling appears sufficient to activate the Heat Shock Response, even in the absence of real damage. In fact, the neuronal release of serotonin facilitates a pre-emptive upregulation of protective genes in the animal, which we have observed to be able to reduce the accumulation of damaged proteins in a C. elegans model of Huntington’s Disease. Additionally, I have seen that anticipating danger can enhance the animal’s stress response in a serotonin-dependent manner, thus facilitating better survival against a subsequent insult that can cause protein damage. Together, these studies present the novel possibility of protection against neurodegenerative disease via modulation of neurotransmission and/or neurosecretion. They also allow for understanding how sensory inputs are coupled to gene expression under stressful conditions. I hope to understand the mechanism by which animals adapt to changes in their environment by coordinating their sensory input with changes in behavior and gene expression.
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Ravula, Surendra Kumar. "A Multielectrode Microcompartment Platform for Signal Transduction in the Nervous System." Diss., Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/11527.

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This dissertation presents the development of a multielectrode microcompartment platform for understanding signal transduction in the nervous system. The design and fabrication of the system and the characterization of the system for pharmacological and electrophysiological measurements of cultured neurons is presented in this work. The electrophysiological activity of cultured dorsal root ganglion (DRG) neurons and cortical neurons is shown on the MEA substrate. These recordings were measured and tied to the toxicological effects of the chemotherapeutic drug vincristine on DRGs. Conventional electrophysiological recordings (via a patch micropipette) are made routinely to record action potentials and ion channel activity in neurons. Moreover, Campenot chambers (traditional compartmented culture systems) have been used for the last thirty years to study the selective application of drugs to neurons. Both of these techniques are useful and well established; however they have their limitations. For instance, Campenot chambers cannot be used very well for small processs-producing neurons, since the barriers are difficult to tranverse. Moreover, conventional patch recordings are labor-intensive, especially when more than one microelectrode needs to be positioned. The developed system is composed of a two compartment divider, each compartment capable of housing axons or cell bodies. Underneath the divider, the substrate has 60 electrodes, arranged in several lines to accommodate several different neurite tracks. Neurons can be stimulated and their activity can be recorded in both of the compartments. The neurotoxin and chemotherapeutic drug vincristine was tested in the system on the DRGs. The drug caused length-dependent axonal degeneration in the DRGs when applied locally. Moreover, electrophysiological activity in both compartments showed that only the activity in the axonal compartment was affected, leading us to believe that the mechanism behind the degeneration is localized to the distal axon.
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Kelps, Kristen. "Molecular and Cellular Characterization of Dopamine Neuron Stimulating Peptides." UKnowledge, 2013. http://uknowledge.uky.edu/neurobio_etds/6.

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Parkinson’s disease, the second most common neurodegenerative disease, is characterized by the loss of dopaminergic neurons within the substantia nigra. Currently, the treatments available for PD are symptomatic treatments that do not stop the progression of the disease. Trophic molecules, such as glial cell-line derived neurotrophic factor (GDNF), have been evaluated as potential therapeutic molecules that could stop the loss of neurons and potentially restore some of the neurons that have already been lost. However, these trophic molecules are large making them difficult to produce and delivery. Here we characterize three peptides (DNSP-5, DNSP-11, and DNSP-17) to determine it they are stable and offer protective effects similar to GNDF allowing them to be potential therapeutic molecules. The data presented here involves the evaluation of the molecular and cellular mechanism of DNSP-5, DNSP-11, and DNSP-17, which are derived from prosequence of GDNF. Initial studies were carried out to evaluate the physical characteristics of these three peptides to determine their viability as potential therapeutic molecules. The structure and stability of these peptides were evaluated. Based on the data it was determined that the three peptides do not interact in vitro, allowing for further individual evaluations of the peptides. It was also determined that the peptides were stable when stored at both -80°C and 37°C for one month, allowing them to both potentially be stored during treatment. Cell culture assays and proteomic profiling were utilized to determine binding partners and potential mechanisms through which DNSP-11 may be able to mediate apoptosis. It was determined that DNSP-11 was able to interact with a variety of binding partners that are involved in metabolism. These studies have aided in the understanding of neurotrophic factor prosequence function, but will also serve as a starting point for the development of novel trophic factors for PD treatment. Finally, the interaction between DNSP-11 and GAPDH was evaluated as a potential anti-apoptotic mechanism. GAPDH has previously shown to play a role in mediating apoptotic pathways. It was hypothesized that the observed interaction between DNSP-11 and GAPDH could mediate that role of GAPDH in apoptosis and afford DNSP-11 its observed anti-apoptotic effects. It was observed that while DNSP-11’s interaction with GAPDH may play a role in its anti-apoptotic effects, it does not appear to be the only mechanism involved. Based on this data, it is likely that the other metabolic binding partners play a role in DNSP-11’s anti-apoptotic mechanisms and therefore, these interactions should be further evaluated.
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May, Verena Elisabeth Luise [Verfasser], and Jürgen [Akademischer Betreuer] Winkler. "Cellular Plasticity within the Central Nervous System of Synucleinopathies / Verena Elisabeth Luise May. Betreuer: Jürgen Winkler." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2013. http://d-nb.info/1035540703/34.

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23

Smith, Nicholas James Chapman. "Neuronopathic Gaucher disease : the pathobiological effects of glucosylsphingosine upon cellular actin within the central nervous system." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648776.

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24

Boone, Jason Nathaniel 1976. "Characterization of novel neural stem cell populations in the Drosophila central nervous system." Thesis, University of Oregon, 2008. http://hdl.handle.net/1794/8160.

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xi, 88 p. A print copy of this thesis is available through the UO Libraries. Search the library catalog for the location and call number.
Neuroblasts are the neural stem cells of the Drosophlia central nervous system. They are large cells that divide asymmetrically to renew another neuroblast and generate a smaller ganglion mother cell (gmc) that will divide once to produce two neurons. Combining genetic lineage tracing experiments with cell fate markers I isolated two separate neural stem cell populations with distinct locations and cellular behaviors in the larval brain. In my first chapter I introduce the central nervous system of Drosophila and in the next two sections of chapter I, I introduce the development of the optic lobe and central brain, two separate structures of the central nervous system. In my second chapter I characterize the lineage relationship of cells within the developing larval optic lobe and use cell fate markers to determine the identity of these cells. Next I examine the effect of spindle orientation on cell fate within epithelial cells of the optic lobe. In my third chapter I characterize another novel neural stem cell lineage in the larval brain containing GMCs with greater proliferation potential than a "canonical" GMC, and I term these, transit amplifying gmcs (TA-GMCs). Further I show that the parent neuroblast of these novel TA-GMCs does not asymmetrically segregate the fate determinant Prospero (Pros) thereby producing a GMC with greater proliferation potential. Finally I show that TA-GMCs do asymmetrically segregate the fate determinant Pros, divide slowly and give rise to up to 10 neurons which normal gmcs never do. In my fourth chapter I show preliminary work on the characterization of a mutation that causes excessive production of neuroblasts specifically in novel TA-GMC lineages. These findings reveal novel neural stem cell lineages, patterns of asymmetric cell division and patterns of neurogenesis that could aid in our understanding of neural stem cell biology and tumorogenesis. This dissertation includes both my previously published and my co-authored materials.
Adviser: Chris Doe
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Zayas, Ventura Ricardo Manuel. "Nitric oxide/cyclic GMP signaling in the central nervous system of Manduca sexta larvae /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2003.

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Thesis (Ph.D.)--Tufts University, 2003.
Adviser: Barry A. Trimmer. Submitted to the Dept. of Biology. Includes bibliographical references (leaves 147-164). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
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Etter, Paul Dezso. "Genomic Approaches to Identifying Transcriptional Targets of AP-1, CREB and JNK Signaling in the Nervous System of Drosophila melanogaster." Diss., Tucson, Arizona : University of Arizona, 2005. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1365%5F1%5Fm.pdf&type=application/pdf.

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27

Sindi, Ghadir A. "Effects of Paternal Obesity on The Central Nervous System Reward Circuitry in Offspring." Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1470232740.

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28

Starck, Laurent [Verfasser], and V. Prasad [Akademischer Betreuer] Shastri. "The new roles of cellular mechanotransduction in mediating astrocyte phenotype and function in the central nervous system." Freiburg : Universität, 2020. http://d-nb.info/1239556365/34.

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29

Zhang, Yi. "Studies of heparanase (HPA) gene expression, cellular localization and functions in neural tissues of the rat." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634061.

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30

Muthukumar, Allie. "Astrocyte-Neuron Interactions Regulate Nervous System Assembly and Function: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/745.

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Astrocytes densely infiltrate the brain and intimately associate with synaptic structures. In the past 20 years, they have emerged as critical regulators of both synapse assembly and synapse function. During development, astrocytes modulate the formation of new synapses, and later, control refinement of synaptic connections in response to activity dependent cues. In a mature nervous system, astrocytes modulate synapse function through a variety of mechanisms. These include ion buffering, neurotransmitter uptake and the release of molecules that activate synaptic receptors. Through such roles, astrocytes shape the structure and function of neuronal circuits. However, how astrocytes and synapses reciprocally communicate during circuit assembly remains an unanswered question in the field. The vast majority of our understanding of astrocyte biology has come from studies conducted in mammals, where it is challenging to dissect molecular mechanisms with cell type specificity. Drosophila melanogaster is a less established model system for studying astrocyteneuron interactions, but its vast array of genetic tools and rapid life cycle promises great potential for precisely targeted manipulations. My thesis work has utilized Drosophila melanogaster to investigate the reciprocal nature of astrocyte-synapse communication. First, I characterized Drosophila late metamorphosis as a developmental stage in which astrocyte-synapse associations can be studied. My work demonstrates that during this time, when the adult Drosophila nervous system is being assembled, synapse formation relies on the coordinated infiltration of astrocyte membranes into the neuropil. Next, I show that in a reciprocal manner, neural activity can shape astrocyte biology during this time as well and impart long lasting effects on neuronal circuit function. In particular expression of the astrocyte GABA transporter (GAT) is modulated in an activity-dependent manner via astrocytic GABABR1/2 receptor signaling. Inhibiting astrocytic GABABR1/2 signaling strongly suppresses hyperexcitability in a Drosophila seizure model, vii arguing this pathway is important for modulating excitatory/inhibitory balance in vivo. Finally, utilizing the ease of the Drosophila system, I performed a reverse genetic screen to identify additional astrocyte factors involved in modulating excitatory-inhibitory neuronal balance.
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31

Muthukumar, Allie. "Astrocyte-Neuron Interactions Regulate Nervous System Assembly and Function: A Dissertation." eScholarship@UMMS, 2001. http://escholarship.umassmed.edu/gsbs_diss/745.

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Astrocytes densely infiltrate the brain and intimately associate with synaptic structures. In the past 20 years, they have emerged as critical regulators of both synapse assembly and synapse function. During development, astrocytes modulate the formation of new synapses, and later, control refinement of synaptic connections in response to activity dependent cues. In a mature nervous system, astrocytes modulate synapse function through a variety of mechanisms. These include ion buffering, neurotransmitter uptake and the release of molecules that activate synaptic receptors. Through such roles, astrocytes shape the structure and function of neuronal circuits. However, how astrocytes and synapses reciprocally communicate during circuit assembly remains an unanswered question in the field. The vast majority of our understanding of astrocyte biology has come from studies conducted in mammals, where it is challenging to dissect molecular mechanisms with cell type specificity. Drosophila melanogaster is a less established model system for studying astrocyteneuron interactions, but its vast array of genetic tools and rapid life cycle promises great potential for precisely targeted manipulations. My thesis work has utilized Drosophila melanogaster to investigate the reciprocal nature of astrocyte-synapse communication. First, I characterized Drosophila late metamorphosis as a developmental stage in which astrocyte-synapse associations can be studied. My work demonstrates that during this time, when the adult Drosophila nervous system is being assembled, synapse formation relies on the coordinated infiltration of astrocyte membranes into the neuropil. Next, I show that in a reciprocal manner, neural activity can shape astrocyte biology during this time as well and impart long lasting effects on neuronal circuit function. In particular expression of the astrocyte GABA transporter (GAT) is modulated in an activity-dependent manner via astrocytic GABABR1/2 receptor signaling. Inhibiting astrocytic GABABR1/2 signaling strongly suppresses hyperexcitability in a Drosophila seizure model, vii arguing this pathway is important for modulating excitatory/inhibitory balance in vivo. Finally, utilizing the ease of the Drosophila system, I performed a reverse genetic screen to identify additional astrocyte factors involved in modulating excitatory-inhibitory neuronal balance.
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32

Bruch, William. "GROUP I METABOTROPIC GLUTAMATE RECEPTORS ON SELECTIVE CELLULAR SUBTYPES IN EPILEPTOGENIC MALFORMED CORTEX." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/378.

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Cortical malformations from altered development are common causes of human epilepsy. The cellular mechanisms responsible for the epileptic state of cortex remain unclear and a significant portion of these cases do not respond to treatment. Previous electrophysiological recordings in the Jacobs lab in a rat polymicrogyria model indicated an increased response to group I metabotropic glutamate receptor agonists in the region adjacent to the malformation (PMZ). In addition there was a novel response in low threshold spiking (LTS) interneurons via mGluR5 activation. To determine whether cell specific expression of these receptors was altered in malformed cortex immunohistochemical stains were performed for group I mGluRs along with non-overlapping interneuron subtype specific markers, a neuronal marker and general inhibitory cell marker. There was no altered mGluR5 expression seen in the PMZ. There was an altered expression seen in PMZ mGluR1α labeled cells and cells in other cortical regions.
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33

Zhang, Yi, and 張怡. "Studies of heparanase (HPA) gene expression, cellular localization andfunctions in neural tissues of the rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634061.

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Mydlarski, Marc Bernard. "Role of the cellular stress response in the biogenesis of redox-active astrocytic inclusions in the aging nervous system." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39970.

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In aging vertebrates, subpopulations of limbic and periventricular astrocytes accumulate peroxidase-positive cytoplasmic inclusions distinct from lipofuscin. In rodent brain, chronic estrogenization accelerates the appearance of this senescent glial phenotype. Identical inclusions are rapidly induced in primary neuroglial cultures by cysteamine exposure. Abnormal mitochondria replete with redox-active iron and other transition metals are the subcellular precursors of the inclusions in situ and in cysteamine-treated cultures. The objective of this thesis was to elucidate mechanisms responsible for the biogenesis of these glial inclusions in the aging nervous system.
We determined that the accumulation of astrocytic inclusions in cysteamine-treated rat glial cultures occurs in the context of an antecedent cellular stress response characterized by (i) the upregulation of heat shock proteins (HSP) 27, 72, 90, ubiquitin and heme oxygenase-1, and (ii) enhanced resistance of cysteamine-stressed astroglia to subsequent oxidative injury. Furthermore, multiple injections of cysteamine or estradiol valerate in adult male rats induced robust overexpression of stress proteins and an accretion of identical peroxidase-positive granules in GFAP-positive astroglia. Both in situ and in cysteamine-treated cultures, HSP27, ubiquitin, glucose-regulated protein 94 and to a lesser extent, HSP72 (but not HSP90 or $ alpha$B-crystallin) exhibited immunolocalization to these astrocytic "stress" inclusions. We observed that exogenous $ rm H sb2O sb2$ induces identical inclusions in cultured astroglia and that cysteamine-derived $ rm H sb2O sb2$ promotes lipid peroxidation in isolated astroglial mitochondria. These data indicate that sustained oxidative stress may represent a "final common pathway" leading to the transformation of normal mitochondria to peroxidase-positive astrocytic inclusions in the aging nervous system.
The metal-dependent peroxidase activity of these glial inclusions has been shown to oxidize dopamine and other catechols to neurotoxic free radicals in vitro, implicating these cells in the pathogenesis of parkinsonism and other free radical-related neurodegenerations. Since peroxidase-positive astroglia have been identified in aging human striatum, the findings presented here suggest that antioxidant therapy coupled with pharmacological inhibition of metal sequestration by "stressed" astroglial mitochondria may prove useful in the management of Parkinson's disease and other age-associated neurodegenerative afflictions.
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35

Ransom, Brian Lyn. "Epidermal growth factor dependent regulation of drosophila nervous system development along the dorso-ventral axis." Thesis, Kansas State University, 2011. http://hdl.handle.net/2097/8772.

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Master of Science
Department of Biology
Tonia L. Von Ohlen
The Drosophila embryonic nervous system develops from an array of neural precursor cells called, neuroblasts. These neuroblasts give rise to all the cell types that populate the mature central nervous system (CNS). The CNS originates from a bilateraly symmetric neurectoderm that is subdivided into three domains along the dorso-ventral (DV) axis. One of these domains is defined by the expression of the Homeodomain protein ventral nervous system defective (vnd). Regulation of neuroblast designation is very precise and controlled. Extensive research has been done on neuroblast formation along the anteroposterior axis, most of which indicates that neuroblast selection within a cluster of neurectodermal cells is controlled by segmentation genes. However, much more research is required to elucidate the function of genes along the DV axis. Early studies indicate that vnd is required for neuroblast formation in the ventral column. Here, we show that vnd function, but not expression, is dependent on MAPK activity downstream of Drosophila EGF-R (DER). Specifically, we show that vnd activity is eliminated in EGF-R mutant embryos in a stage specific manner by evaluating vnd’s ability to inhibit intermediate neuroblast defective (ind), muscle segment homeobox (msh), and the newly identified neural tube development player, neu3. Finally, we show that DER functionality in the ventral column is entirely dependent on the processing protein rhomboid (rho) in later stage embryos.
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36

Caprariello, Andrew Vincent. "Cytoarchitectural Defects Secondary To Experimentally Induced Oligodendrocyte Death In The Adult And Developing Central Nervous System." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1346859526.

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37

Chidambaram, Archana. "WILMS’ TUMOR-1 (WT1) PROTEIN EXPRESSION IN GLIOMA CELLS ACTUATES CELLULAR INVASIVENESS- IDENTIFYING ITS TARGET GENES." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2454.

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Previous studies in our laboratory demonstrated the expression of WT1 in a significant number of glioma cells and established its role in promoting tumor cell proliferation. Here, we noted the effect(s) of manipulating WT1 levels on the expression levels of genes that were previously shown to be regulated by WT1. We found no correlation between the expression levels of WT1 and PDGF-A, Snai1 and E-cadherin and a consistent inverse correlation between WT1 and IGF-1R expression in U251-MG cells. To ascertain whether the increased IGF-1R levels resulting from WT1 silencing could account for decreased cellular proliferation, we utilized siRNA mediated knockdown of IGF-1R and found a modest decrease in cellular proliferation. Gene expression profiling in U251-MG cells was then used to identify candidate target genes for WT1. Several genes whose levels directly correlated with WT1 were observed to have putative or established oncogenic role(s) in glioma cells or other malignancies. Among the genes correlated inversely, meanwhile, a tumor-suppressor role was attributed to some. Real time RT-PCR helped to substantiate these microarray findings in U251-MG cells. We also characterized the expression and function of WT1 in U1242-MG and GBM6 cells. Interestingly, in these cells WT1 facilitated cell invasiveness but had no discernible influence on cellular proliferation. The expressions of the candidate WT1 target genes were studied also determined in these 2 cell lines. At least 3 genes were consistently down-regulated with WT1 silencing in the three cell lines- INPP5A, CD97, and TYMS. To determine whether CD97 assisted WT1 in facilitating cellular invasion, we silenced CD97 expression using siRNA and noted a significant decrease in the cells’ ability to invade through Matrigel-coated filters. We propose that WT1 profoundly impacts the glioma cells’ invasive ability, and this function is mediated by CD97 alone or in conjunction with other pro-invasive molecules. Our findings argue for the oncogenic role of WT1 in the specific context of glioma cells. They also point to a novel pro-invasive protein- CD97- in glioma cells. Further studies are necessary to confirm the mechanism by which CD97 promotes invasion as well as to explore its potential as a diagnostic and/or therapeutic target.
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Diao, Tiemei, and 刁鈇梅. "The gene expression, binding properties and intracelular signal transduction of kappa-opioid receptor in non-neuronal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31220770.

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39

Poon, Hiu-ching. "A study of the regulatory roles of Hedgehog in the enteric nervous system development by the conditional knockout of Patched1 enteric gene in the enteric neural crest cells." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42841604.

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40

Pan, Feng. "Understanding Ten-Eleven Translocation-2 in Hematological and Nervous Systems." FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1925.

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I proposed the study of two distinct aspects of Ten-Eleven Translocation 2 (TET2) protein for understanding specific functions in different body systems. In Part I, I characterized the molecular mechanisms of Tet2 in the hematological system. As the second member of Ten-Eleven Translocation protein family, TET2 is frequently mutated in leukemic patients. Previous studies have shown that the TET2 mutations frequently occur in 20% myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN), 10% T-cell lymphoma leukemia and 2% B-cell lymphoma leukemia. Genetic mouse models also display distinct phenotypes of various types of hematological malignancies. I performed 5-hydroxymethylcytosine (5hmC) chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA sequencing (RNA-Seq) of hematopoietic stem/progenitor cells to determine whether the deletion of Tet2 can affect the abundance of 5hmC at myeloid, T-cell and B-cell specific gene transcription start sites, which ultimately result in various hematological malignancies. Subsequent Exome sequencing (Exome-Seq) showed that disease-specific genes are mutated in different types of tumors, which suggests that TET2 may protect the genome from being mutated. The direct interaction between TET2 and Mutator S Homolog 6 (MSH6) protein suggests TET2 is involved in DNA mismatch repair. Finally, in vivo mismatch repair studies show that the loss of Tet2 causes a mutator phenotype. Taken together, my data indicate that TET2 binds to MSH6 to protect genome integrity. In Part II, I intended to better understand the role of Tet2 in the nervous system. 5-hydroxymethylcytosine regulates epigenetic modification during neurodevelopment and aging. Thus, Tet2 may play a critical role in regulating adult neurogenesis. To examine the physiological significance of Tet2 in the nervous system, I first showed that the deletion of Tet2 reduces the 5hmC levels in neural stem cells. Mice lacking Tet2 show abnormal hippocampal neurogenesis along with 5hmC alternations at different gene promoters and corresponding gene expression downregulation. Through the luciferase reporter assay, two neural factors Neurogenic differentiation 1 (NeuroD1) and Glial fibrillary acidic protein (Gfap) were down-regulated in Tet2 knockout cells. My results suggest that Tet2 regulates neural stem/progenitor cell proliferation and differentiation in adult brain.
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Glossop, Nicholas Robert John. "The developmental assembly of sensory axon arrays in the nervous system of Drosophila melanogaster : a combined cellular, genetic and molecular study." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241942.

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Chou, Chiu-wen, and 周秋雯. "A study of the expression of NF-kB in central nervous system of rats with neuropathic pain." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44902542.

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43

Ellis, Rebecca Catherine. "Characterization of cathepsin b mrna and protein expression, enzymatic activity and cellular localization following contusion spinal cord injury in rats." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0007160.

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Thesis (Ph.D.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 97 pages. Includes Vita. Includes bibliographical references.
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Holler, Christopher J. "THE CELLULAR NUCLEIC ACID BINDING PROTEIN REGULATES THE ALZHEIMER’S DISEASE β-SECRETASE PROTEIN BACE1." UKnowledge, 2012. http://uknowledge.uky.edu/biochem_etds/12.

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Alzheimer’s disease (AD) is the most common neurodegenerative disease affecting the elderly population and is believed to be caused by the overproduction and accumulation of the toxic amyloid beta (Aβ) peptide in the brain. Aβ is produced by two separate enzymatic cleavage events of the larger membrane bound amyloid precursor protein, APP. The first, and rate-limiting, cleavage event is made by beta-secretase, or BACE1, and is thus an attractive therapeutic target. Our lab, as well as many others, has shown that BACE1 protein and activity are increased in late-stage sporadic AD. We have extended these findings to show that BACE1 is increased in the earliest stages of AD before the onset of significant Aβ accumulation, indicating a potential causal role in the disease. Interestingly, BACE1 mRNA levels are unchanged in AD, leading to reason that a post-transcriptional method of BACE1 regulation is altered in disease. To date, the mechanism for this aberrant post-transcriptional regulation has not been elucidated. This study has implicated the cellular nucleic acid binding protein (CNBP), a highly conserved RNA binding protein, as a positive regulator of BACE1 translation, with implications for the etiology of sporadic AD. CNBP overexpression in cultured cells or spiked into a cell-free in vitro translation system increased BACE1 protein expression without affecting BACE1 mRNA levels. Knockdown of CNBP reduced BACE1 protein and mRNA slightly. Furthermore, CNBP associated with BACE1 mRNA in cell lysates and bound directly to the BACE1 5’ UTR in vitro, which confers most of the regulatory activity. Importantly, CNBP was increased in the progression of AD and correlated with BACE1 expression. Cellular stressors (such as glucose deprivation and oxidative stress) that occur in the AD brain increase BACE1 translation and we have found that these stressors increased CNBP expression as well. Early experimental evidence suggests that CNBP may enhance BACE1 translation through a cap-independent mechanism, which is an alternative translational pathway activated by cell stress. These studies indicate that the RNA binding protein CNBP is a novel trans-acting factor important for the regulation of BACE1 protein production and may be a viable therapeutic target for AD.
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Oliver, Devyn. "Constructing and Maintaining the Nervous System: Molecular Insights Underlying Neuronal Architecture, Synaptic Development, and Synaptic Maintenance Using C. elegans." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1123.

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In the nervous system, billions of neurons undergo a multistep process to establish functional circuits. This entails accurate extension of dendritic and axonal processes and coordinated efforts of pre- and postsynaptic neurons to form synaptic connections. Although many axon guidance molecules and synaptic organizers have been identified, the molecular redundancy and the vast number of synapses in the brain has complicated attempts to define their precise roles. In order to understand the molecular mechanisms that encompass these processes, my studies utilize the genetic strengths and cellular precision available in Caenorhabditis elegans for in vivo investigations of nervous system development. In this work, I unravel cell-specific requirements for the transmembrane receptor integrin in regulating developmental axon guidance of GABAergic motor neurons. Furthermore, I address important questions about mechanisms of synapse formation and maintenance using a novel dendritic spine model in C. elegans. Using high resolution microscopy, I find that the formation of immature presynaptic vesicles and postsynaptic receptors are established prior to the outgrowth of dendritic spines at nascent synapses. During this early period of synapse formation, the kinesin-3 family protein UNC-104/KIF1A transports a transsynaptic adhesion molecule neurexin/NRX-1 to developing active zones, in order to maintain postsynaptic receptors and dendritic spines in the mature circuit. In the absence of nrx-1, spines initially form normally but collapse following their extension. These findings demonstrate that presynaptic NRX-1 is required to maintain postsynaptic structures. Together my work provides new insights into molecular mechanisms that define spatiotemporal characteristics of nervous system development and the maintenance of connectivity.
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46

Poon, Hiu-ching, and 潘曉澄. "A study of the regulatory roles of Hedgehog in the enteric nervous system development by the conditional knockout of Patched1 entericgene in the enteric neural crest cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42841604.

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Smith, Angeline Gabriel. "Cellular and molecular studies upon repair and regeneration within the nervous system of asexually dividing tetrathyridia of mesocestoides vogae (Syn. M. corti)." Thesis, University of Ulster, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.232840.

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48

Tischbein, Maeve. "FUS and Excitotoxicity Cross Paths in ALS: New Insights into Cellular Stress and Disease." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/990.

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Amyotrophic lateral sclerosis (ALS) is an incurable and fatal neurodegenerative disease characterized by motor neuron loss. Although pathological mutations exist in >15 genes, the mechanism(s) underlying ALS are unknown. FUS is one such gene and encodes the nuclear RNA-binding protein (RBP), fused in sarcoma (FUS), which actively shuttles between the nucleus and cytoplasm. Intriguingly, nearly half of the ALS mutations identified in FUS cause this protein to mislocalize, suggesting that FUS localization is relevant to disease. Here, we found that excitotoxicity, a neuronal stress caused by aberrant glutamate signaling, induces the rapid redistribution of FUS and additional disease-linked RBPs from the nucleus to the cytoplasm. As excitotoxicity is pathologically associated with ALS, it was notable that the nuclear egress of FUS was particularly robust. Further, ALS-FUS variants that predominantly localize to the nucleus also undergo redistribution. Thus, we sought to understand the purpose underlying FUS translocation and the potential relevance of this response to disease. As calcium dysregulation is strongly associated with neurodegenerative disorders, we examined the contribution of calcium to FUS egress. In addition to global changes to nucleocytoplasmic transport following excitotoxic insult, we observed that FUS translocation caused by excitotoxicity is calcium mediated. Moreover, we found that dendritic expression of Gria2, a transcript encoding an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit responsible for regulating calcium permeability, is FUS-dependent under conditions of stress. Together, these observations support the premise that FUS has a normal function during excitotoxic stress and that glutamatergic signaling may be dysregulated in FUS-mediated ALS.
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49

Hebbar, Sarita. "Patterning the DLM innervation in Drosophila: cellular interactions and molecular mechanisms." Miami University / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=miami1123793870.

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50

Dallimore, Elizabeth Jane. "Molecular and cellular characteristics of early vs late born retinal ganglion cells." University of Western Australia. School of Anatomy and Human Biology, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0138.

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[Truncated abstract] Developmentally, the rodent retinocollicular projection is often thought of as a homogenous projection of retinal ganglion cell (RGC) axons, however the extensive period of RGC neurogenesis and sequential arrival of their axons into central targets such as the superior colliulus (SC) suggests otherwise. RGC axons are already present in the developing SC at embryonic (E) day 16.5-17. RGCs born on E15 have innervated the SC by birth, whereas axons derived from RGCs that are born last (E19) do not grow into the SC until postnatal (P) days 4-6 (Dallimore et al., 2002). These observations may go someway to explaining why, after SC lesions in rats at P2, there is greater growth distal to the lesion site compared to lesions made at P6 (Tan and Harvey, 1997b). It may be that the post lesion growth is simply de novo growth of axons from late-born RGCs rather than regeneration of pre-existing, injured axons. Early and late cohorts of growing RGC axons presumably encounter different developmental terrains as they grow from retina to central targets, possibly resulting in differences in developmental milestones and growth potentials. There may also be differences in guidance cues, further suggesting that gene expression in early vs late born RGCs may differ. To examine differences between early (E15) and late (E19) born RGCs during development, the time-course and extent of programmed RGC death in normal rat pups, and RGC death following the removal of target-derived trophic factors, was assessed. ... On the other hand, LCM captured GCL analysed for gene expression at P0 and P7 revealed decreases in AKT, Math5, Notch1, c-jun, DCC, Arginase-1 mRNA levels and a considerable decrease in GAP-43 expression. It is not surprising to see differences in gene expression between whole eye and the more specific GCL samples, as the cells in all layers of the retina have very different functions and different developmental profiles. It is important to note decreases in mRNA expression in the GCL for a number of the genes analysed at P0 and P7, reflecting cessation of RGC death and completion of axonal growth into central visual targets. I also examined at the protein level expression of DCC, Arginase1, c-Jun and Bcl-2 at birth (P0) in BrdU labeled RGCs born on E15 or E19. When comparing the percentage of double labelled cells compared to the total number of cells expressing each protein, Bcl-2, c-Jun and Arg1 were expressed more in E15 RGCs (22.90%, 72.71%, and 16.44% respectively in E15 RGCs, compared with 0.52%, 13.17% and 3.59% in E19 RGCs). In contrast, DCC was expressed more at birth in E19 RGCs (18.05% in E19 RGCs compared with 9.23% in E15 RGCs). This shows there is clearly a difference in the expression of proteins in the two cohorts of RGCs, which is consistent with PCR data and with their growth state as their axons encounter the changes in the newborn brain. The overall findings of this research suggest that seemingly homogenous populations of neurons are quite different in their developmental profile and in their response to injury. This work may provide new ways of determining better strategies for CNS repair and the most effective way of targeting cells for regeneration and survival.
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