subject:(Central Nervous System physiology)

Bond University

1. Juneja, Rita. Mechanisms of Axonal Regeneration After Central Nervous System Injury.

Degree: 2012, Bond University

URL: https://epublications.bond.edu.au/theses/112

► The adult zebrafish was used as a model for investigating neurite regeneration and to determine how different substrates and promoting factors contribute to the neurite… (more)

Subjects/Keywords: Central nervous system Regeneration; Axons physiology; Zebrafish; Central Nervous System physiology; Nerve Regeneration physiology.; Biology, Cell (0379)

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APA (6^th Edition):

Juneja, R. (2012). Mechanisms of Axonal Regeneration After Central Nervous System Injury. (Thesis). Bond University. Retrieved from https://epublications.bond.edu.au/theses/112

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Juneja, Rita. “Mechanisms of Axonal Regeneration After Central Nervous System Injury.” 2012. Thesis, Bond University. Accessed March 05, 2021. https://epublications.bond.edu.au/theses/112.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Juneja, Rita. “Mechanisms of Axonal Regeneration After Central Nervous System Injury.” 2012. Web. 05 Mar 2021.

Vancouver:

Juneja R. Mechanisms of Axonal Regeneration After Central Nervous System Injury. [Internet] [Thesis]. Bond University; 2012. [cited 2021 Mar 05]. Available from: https://epublications.bond.edu.au/theses/112.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Juneja R. Mechanisms of Axonal Regeneration After Central Nervous System Injury. [Thesis]. Bond University; 2012. Available from: https://epublications.bond.edu.au/theses/112

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Michigan State University

2. Nikundiwe, Alfeo Mauya, 1938-. The ontogeny of coordinated limb movements in pre-hatched chicks : effects of central nervous system manipulations on the frequency and patterns of movements.

Degree: PhD, Department of Zoology, 1972, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:25151

Subjects/Keywords: Central nervous system; Poultry – Physiology

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APA (6^th Edition):

Nikundiwe, Alfeo Mauya, 1. (1972). The ontogeny of coordinated limb movements in pre-hatched chicks : effects of central nervous system manipulations on the frequency and patterns of movements. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:25151

Chicago Manual of Style (16^th Edition):

Nikundiwe, Alfeo Mauya, 1938-. “The ontogeny of coordinated limb movements in pre-hatched chicks : effects of central nervous system manipulations on the frequency and patterns of movements.” 1972. Doctoral Dissertation, Michigan State University. Accessed March 05, 2021. http://etd.lib.msu.edu/islandora/object/etd:25151.

MLA Handbook (7^th Edition):

Nikundiwe, Alfeo Mauya, 1938-. “The ontogeny of coordinated limb movements in pre-hatched chicks : effects of central nervous system manipulations on the frequency and patterns of movements.” 1972. Web. 05 Mar 2021.

Vancouver:

Nikundiwe, Alfeo Mauya 1. The ontogeny of coordinated limb movements in pre-hatched chicks : effects of central nervous system manipulations on the frequency and patterns of movements. [Internet] [Doctoral dissertation]. Michigan State University; 1972. [cited 2021 Mar 05]. Available from: http://etd.lib.msu.edu/islandora/object/etd:25151.

Council of Science Editors:

Nikundiwe, Alfeo Mauya 1. The ontogeny of coordinated limb movements in pre-hatched chicks : effects of central nervous system manipulations on the frequency and patterns of movements. [Doctoral Dissertation]. Michigan State University; 1972. Available from: http://etd.lib.msu.edu/islandora/object/etd:25151

Euskal Herriko Unibertsitatea / Universidad del País Vasco

3. Navalpotro Gómez, Irene. Mecanismos fisiopatólogicos del Trastorno de control de Impulsos en la enfermedad de Parkinson .

Degree: 2019, Euskal Herriko Unibertsitatea / Universidad del País Vasco

URL: http://hdl.handle.net/10810/39723

► La presente tesis se ha centrado en el estudio de los mecanismos fisiopatológicos del trastorno de control de impulsos (TCI) en pacientes con enfermedad de… (more)

▼ La presente tesis se ha centrado en el estudio de los mecanismos fisiopatológicos del trastorno de control de impulsos (TCI) en pacientes con enfermedad de Parkinson (EP). El TCI es una complicación relevante ya que es frecuente y grave en muchas ocasiones, comportando una elevada disrupción de la vida del paciente y su entorno que puede llevar hasta al suicidio en los casos más graves. A pesar de las importantes repercusiones, sus mecanismos fisiopatológicos son desconocidos, habiéndose descrito resultados contradictorios a múltiples niveles de estudio, pero especialmente en los estudios de imagen. Esta tesis se ha realizado no sólo con el ánimo de comprender los mecanismos por los que ocurre, sino también con el objetivo de ampliar las herramientas de detección de los sujetos que serán más sensibles al desarrollo de esta complicación tras el inicio de la terapia de reposición dopaminérgica. Por este motivo, se ha realizado en estos pacientes una aproximación multimodal de neuroimagen desde diversas técnicas, con el objetivo de entender la interacción entre el impacto de la degeneración dopaminérgica y elreemplazo terapéutico en aspectos críticos del comportamiento humano, contribuyendo a delinear los posibles correlatos neurales relacionados con esta complicación en los pacientes con EP. El hecho de investigar y profundizar en los circuitos cerebrales que se encuentran alterados en este tipo de pacientes, podría abrir una puerta a la hora de tratar esta complicación una vez establecida, quizá fundamentando las bases de la terapia con ECP con electrodos direccionales y otros tratamientos focalizados en áreas pertenecientes al circuito límbico. Este trabajo también contribuiría al descubrimiento de biomarcadores de neuroimagen que pudiesen identificar pacientes con EP susceptibles de desarrollar un TCI, con el objetivo de su prevención evitando terapias con agonistas dopaminérgicos en dichos casos. Esta tesis se divide en tres subapartados en las que en (i) el primero estudiamos el patrón de denervación dopaminérgica de estos pacientes así como su asociación con el metabolismo cerebral y con diferentes características clínicas y cognitivas. Esto ha dado lugar a un artículo ya publicado en Eur J Nucl Med Mol Imaging. (ii) En segundo lugar se ha investigado la conectividad funcional dinámica en la Resonancia Magnética funcional en reposo en estos pacientes así como las propiedades topológicas de la misma mediante un análisis de teoría de grafos. Este artículo está actualmente en revisión por la revista Parkinsonism and related disorders journal. (iii) Por último en estos pacientes se ha estudiado la activación cerebral, el curso temporal de la misma y la mediación de la conectividad funcional mientras estos pacientes se enfrentaban en la Resonancia Magnética funcional al Juego de Azar de Iowa, una tarea de toma de decisiones y de control inhibitorio.Resumiendo los resultados: el estudio de la denervación dopaminérgica estriatal, muestra en estos pacientes una denervación dopaminérgica en el estriado ventral… Advisors/Committee Members: Rodríguez Oroz, Mari Cruz (advisor), Grandes Moreno, Pedro Rolando (advisor).

Subjects/Keywords: physiology of the central nervous system; neurology; fisiología del sistema nervioso central; neurología

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APA (6^th Edition):

Navalpotro Gómez, I. (2019). Mecanismos fisiopatólogicos del Trastorno de control de Impulsos en la enfermedad de Parkinson . (Doctoral Dissertation). Euskal Herriko Unibertsitatea / Universidad del País Vasco. Retrieved from http://hdl.handle.net/10810/39723

Chicago Manual of Style (16^th Edition):

Navalpotro Gómez, Irene. “Mecanismos fisiopatólogicos del Trastorno de control de Impulsos en la enfermedad de Parkinson .” 2019. Doctoral Dissertation, Euskal Herriko Unibertsitatea / Universidad del País Vasco. Accessed March 05, 2021. http://hdl.handle.net/10810/39723.

MLA Handbook (7^th Edition):

Navalpotro Gómez, Irene. “Mecanismos fisiopatólogicos del Trastorno de control de Impulsos en la enfermedad de Parkinson .” 2019. Web. 05 Mar 2021.

Vancouver:

Navalpotro Gómez I. Mecanismos fisiopatólogicos del Trastorno de control de Impulsos en la enfermedad de Parkinson . [Internet] [Doctoral dissertation]. Euskal Herriko Unibertsitatea / Universidad del País Vasco; 2019. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10810/39723.

Council of Science Editors:

Navalpotro Gómez I. Mecanismos fisiopatólogicos del Trastorno de control de Impulsos en la enfermedad de Parkinson . [Doctoral Dissertation]. Euskal Herriko Unibertsitatea / Universidad del País Vasco; 2019. Available from: http://hdl.handle.net/10810/39723

University of the Western Cape

4. Kadernani, Yakub Esmail Y.E. Novel adamantane derivatives as multifunctional neuroprotective agents .

Degree: 2013, University of the Western Cape

URL: http://hdl.handle.net/11394/4256

► The pathology of neurodegenerative disorders involves multiple steps, and it is probably for this reason that targeting one particular step in a multi-step process has… (more)

▼ The pathology of neurodegenerative disorders involves multiple steps, and it is probably for this reason that targeting one particular step in a multi-step process has only yielded limited results. Nitric oxide (NO) is synthesised from L-Arginine by an enzyme known as nitric oxide synthase (NOS). Three isoforms of NOS exist, including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). In the central nervous system (CNS), nNOS is involved in the synthesis of NO, which is involved in various neurological functions. NO is a free radical and this probably explains why an excess amount of it has been implicated in the development of neurodegenerative disorders. In the CNS, the Nmethyl- D-aspartate (NMDA) receptor in its active state allows the influx of calcium ions which activate nNOS thus increasing the amount of NO and other detrimental reactive nitrogen species within neuronal cells. Calcium entry through voltage-gated calcium channels (VGCC) may also contribute to this. Although calcium ions are important for physiological functioning, an excess is responsible for excitotoxicity, which can ultimately lead to neurodegeneration. Our aim was to synthesise a series of adamantane-derived compounds that act at multiple target sites in the neurodegenerative pathway. By conjugating benzyl and phenylethyl moieties with different functional groups (-H, -NO2, -NH2, -NHC(NH)NH2, -OCH3) to the amantadine structure, we aimed to synthesise compounds that display calcium channel and NMDA receptor (NMDAR) channel inhibition, as well as selective inhibition of nNOS. A series of compounds (-H, -NO2, -NH2, -OCH3) were obtained in yields that varied between 16.5 % and 90.25 %. These novel compounds were tested for calcium influx through VGCC and NMDAR inhibition using synaptoneurosomes isolated from rat brain homogenate against the reference compounds MK-801, NGP1-01, amantadine, memantine and nimodipine. A lack of success with the synthesis of the guanidine compounds prevented the use of the oxyhemoglobin capture assay for the determination of nNOS inhibitory activity of these compounds. The novel synthesised compounds display inhibitory activity towards VGCC and the NMDAR in the micromolar range. Further tests are recommended on compounds SE-1, SE-4, SE-11 and SE-12 as they displayed good inhibitory activity against both NMDAR- as well as ii KCl-mediated calcium influx. These novel compounds may be better therapeutic options than amantadine and memantine as they inhibit both NMDAR and VGCC-mediated calcium influx, whereas amantadine and memantine only inhibit NMDA-mediated calcium influx. These novel adamantane derived compounds may possibly serve as novel leads or potential therapeutic agents for the treatment of neurodegenerative disorders. Advisors/Committee Members: Joubert, J (advisor).

Subjects/Keywords: Neurodegenerative disorders; Central nervous system

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APA (6^th Edition):

Kadernani, Y. E. Y. E. (2013). Novel adamantane derivatives as multifunctional neuroprotective agents . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/4256

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kadernani, Yakub Esmail Y E. “Novel adamantane derivatives as multifunctional neuroprotective agents .” 2013. Thesis, University of the Western Cape. Accessed March 05, 2021. http://hdl.handle.net/11394/4256.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kadernani, Yakub Esmail Y E. “Novel adamantane derivatives as multifunctional neuroprotective agents .” 2013. Web. 05 Mar 2021.

Vancouver:

Kadernani YEYE. Novel adamantane derivatives as multifunctional neuroprotective agents . [Internet] [Thesis]. University of the Western Cape; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/11394/4256.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kadernani YEYE. Novel adamantane derivatives as multifunctional neuroprotective agents . [Thesis]. University of the Western Cape; 2013. Available from: http://hdl.handle.net/11394/4256

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Montana State University

5. Waller, Hannah Rose. Analysis of the central nervous system in a mouse model of HSAN Type III.

Degree: MS, College of Letters & Science, 2013, Montana State University

URL: https://scholarworks.montana.edu/xmlui/handle/1/3026

► Familial Dysautonomia (FD), also called Riley Day Syndrome, is a Hereditary Sensory and Autonomic Neuropathy (HSAN Type III) that is characterized by dysfunction of the… (more)

▼ Familial Dysautonomia (FD), also called Riley Day Syndrome, is a Hereditary Sensory and Autonomic Neuropathy (HSAN Type III) that is characterized by dysfunction of the sensory and autonomic nervous systems. The disease is caused by a severe reduction in levels of the protein IKAP as a result of a point mutation in Ikbkap mRNA which results in targeting of the mRNA for nonsense mediated decay. In humans, symptoms include autonomic crises, tachycardia, blood pressure lability, lack of overflow tears, decreased pain and temperature sensation, and scoliosis. Half of affected individuals die by age 40. Although FD has been traditionally classified as a disease of the autonomic nervous system, there have been notable effects observed in the central nervous system (CNS) as well, though many of these observations remain to be quantified. The presented study evaluated the impact of FD on the CNS using a mouse model where Ikbkap was deleted selectively from neurons of the CNS. For this model, a conditional knockout (CKO) strategy was employed because mice that are null for Ikbkap die by embryonic day 10.5, precluding their usefulness for analyzing FD in the adult CNS. For this study, morphological analyses and immunohistochemical staining were performed on the brain tissue. Affected mice were found to have a significant reduction in choline acetyltransferase (ChAT) positive neurons in the dorsal motor nucleus of the vagus nerve (DMNX) relative to controls, indicating potential decreased parasympathetic innervation of the nucleus in the heart and other target organs. Additionally, the size of the lateral ventricles and hippocampus relative to hemisphere size was significantly increased for the mutant mice. Further, the corpus callosum and lateral amygdaloid nucleus areas were significantly decreased relative to wild-type controls. Cortical layering was found to be normal in Talpha1tubulin-Cre/Ikbkap CKO mice. Taken together, these results suggest that the morphological differences are associated with increased cell death and decreased neurogenesis and cell differentiation. The neural and morphological findings presented in this study are the first data demonstrating perturbations in the CNS of a mouse model for FD and may explain some of the phenotypes observed in FD patients. Advisors/Committee Members: Chairperson, Graduate Committee: Frances Lefcort (advisor).

Subjects/Keywords: Dysautonomia.; Central nervous system.

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APA (6^th Edition):

Waller, H. R. (2013). Analysis of the central nervous system in a mouse model of HSAN Type III. (Masters Thesis). Montana State University. Retrieved from https://scholarworks.montana.edu/xmlui/handle/1/3026

Chicago Manual of Style (16^th Edition):

Waller, Hannah Rose. “Analysis of the central nervous system in a mouse model of HSAN Type III.” 2013. Masters Thesis, Montana State University. Accessed March 05, 2021. https://scholarworks.montana.edu/xmlui/handle/1/3026.

MLA Handbook (7^th Edition):

Waller, Hannah Rose. “Analysis of the central nervous system in a mouse model of HSAN Type III.” 2013. Web. 05 Mar 2021.

Vancouver:

Waller HR. Analysis of the central nervous system in a mouse model of HSAN Type III. [Internet] [Masters thesis]. Montana State University; 2013. [cited 2021 Mar 05]. Available from: https://scholarworks.montana.edu/xmlui/handle/1/3026.

Council of Science Editors:

Waller HR. Analysis of the central nervous system in a mouse model of HSAN Type III. [Masters Thesis]. Montana State University; 2013. Available from: https://scholarworks.montana.edu/xmlui/handle/1/3026

6. Bellot-Saez, Alba. Astrocytic modulation of neuronal network oscillations.

Degree: 2019, Western Sydney University

URL: http://hdl.handle.net/1959.7/uws:54319

► The synchronization of the neuron’s membrane potential results in the emergence of neuronal oscillations at multiple frequencies that serve distinct physiological functions (e.g. facilitation of… (more)

▼ The synchronization of the neuron’s membrane potential results in the emergence of neuronal oscillations at multiple frequencies that serve distinct physiological functions (e.g. facilitation of synaptic plasticity) and correlate with different behavioural states (e.g. sleep, wakefulness, attention). It has been postulated that at least ten distinct mechanisms are required to cover the large frequency range of neuronal oscillations in the cortex, including variations in the concentration of extracellular neurotransmitters and ions, as well as changes in cellular excitability. However, the mechanism that gears the transition between different oscillatory frequencies is still unknown. Over the past decade, astrocytes have been the focus of much research, mainly due to (1) their close association with synapses forming what is known today as the “tripartite synapse”, which allows them to bidirectionally interact with neurons and modulate synaptic transmission; (2) their syncytium-like activity, as they are electrically coupled via gap junctions and actively communicate through Ca2+ waves; and (3) their ability to regulate neuronal excitability via glutamate uptake and tight control of the extracellular K+ levels via a process termed K+ clearance. In this thesis we hypothesized that astrocytes, in addition to their role as modulators of neuronal excitability, also act as “network managers” that can modulate the overall network oscillatory activity within their spatial domain. To do so, it is proposed that astrocytes fine-tune their K+ clearance capabilities to affect neuronal intrinsic excitability properties and synchronization with other neurons, thus mediating the transitions between neuronal network oscillations at different frequencies. To validate or reject this hypothesis I have investigated the potential role of astrocytes in modulating cortical oscillations at both cellular and network levels, aiming at answering three main research questions: a) what is the impact of alterations in astrocytic K+ clearance mechanisms on cortical networks oscillatory dynamics? b) what specific neuronal properties underlying the generation of neuronal oscillations are affected as a result of impairments in the astrocytic K+ clearance process? and c) what are the bidirectional mechanisms between neurons and astrocytes (i.e. neuromodulators) that specifically affect the K+ clearance process to modulate the network activity output? In the first experimental chapter I used electrophysiological recordings and pharmacological manipulations to dissect the contribution of the different astrocytic K+ clearance mechanisms to the modulation of neuronal network oscillations at multiple frequencies. A key finding was that alterations in membrane properties of layer V pyramidal neurons strongly correlated with the network behaviour following impairments in astrocytic K+ clearance capabilities, depicted as enhanced excitability underlying the amplification of high-frequency oscillations, especially within the beta and gamma range. The second… Advisors/Committee Members: Western Sydney University. School of Medicine (Host institution).

Subjects/Keywords: astrocytes; central nervous system; diseases; neurons; physiology; neural transmission; Thesis (Ph.D.) – Western Sydney University, 2019

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APA (6^th Edition):

Bellot-Saez, A. (2019). Astrocytic modulation of neuronal network oscillations. (Thesis). Western Sydney University. Retrieved from http://hdl.handle.net/1959.7/uws:54319

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bellot-Saez, Alba. “Astrocytic modulation of neuronal network oscillations.” 2019. Thesis, Western Sydney University. Accessed March 05, 2021. http://hdl.handle.net/1959.7/uws:54319.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bellot-Saez, Alba. “Astrocytic modulation of neuronal network oscillations.” 2019. Web. 05 Mar 2021.

Vancouver:

Bellot-Saez A. Astrocytic modulation of neuronal network oscillations. [Internet] [Thesis]. Western Sydney University; 2019. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1959.7/uws:54319.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bellot-Saez A. Astrocytic modulation of neuronal network oscillations. [Thesis]. Western Sydney University; 2019. Available from: http://hdl.handle.net/1959.7/uws:54319

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Montana

7. Webster, W. Wallace. Differential sensitivity of high-affinity glutamate transport systems to oxidative stress.

Degree: MS, 1998, University of Montana

URL: https://scholarworks.umt.edu/etd/2070

Subjects/Keywords: Stress (Physiology); Central nervous system; Neurotransmitters

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APA (6^th Edition):

Webster, W. W. (1998). Differential sensitivity of high-affinity glutamate transport systems to oxidative stress. (Masters Thesis). University of Montana. Retrieved from https://scholarworks.umt.edu/etd/2070

Chicago Manual of Style (16^th Edition):

Webster, W Wallace. “Differential sensitivity of high-affinity glutamate transport systems to oxidative stress.” 1998. Masters Thesis, University of Montana. Accessed March 05, 2021. https://scholarworks.umt.edu/etd/2070.

MLA Handbook (7^th Edition):

Webster, W Wallace. “Differential sensitivity of high-affinity glutamate transport systems to oxidative stress.” 1998. Web. 05 Mar 2021.

Vancouver:

Webster WW. Differential sensitivity of high-affinity glutamate transport systems to oxidative stress. [Internet] [Masters thesis]. University of Montana; 1998. [cited 2021 Mar 05]. Available from: https://scholarworks.umt.edu/etd/2070.

Council of Science Editors:

Webster WW. Differential sensitivity of high-affinity glutamate transport systems to oxidative stress. [Masters Thesis]. University of Montana; 1998. Available from: https://scholarworks.umt.edu/etd/2070

East Carolina University

8. Johnson, Tracy L. Dopaminergic modulation of the autonomic nervous system: in vitro and in vivo evidence from the mouse.

Degree: MS, Biomedical Sciences, 2012, East Carolina University

URL: http://hdl.handle.net/10342/4015

► Central nervous system (CNS) function depends on both the connections between the underlying neurons and neural circuits and their activity. Neuronal activity in turn can… (more)

▼ Central nervous system (CNS) function depends on both the connections between the underlying neurons and neural circuits and their activity. Neuronal activity in turn can be classified as neurotransmission and neuromodulation, where neuromodulation serves as a means to adapt neurotransmission to the different behavioral needs of the animal. Here, using the well-described monosynaptic stretch reflex (MSR) spinal circuit as a tool, we compared in the in vitro mouse spinal cord preparation the modulatory actions of DA in spinal lumbar segments that mediate somatosensory input and locomotor output with segments that additionally house the final common output of the autonomic nervous system (ANS). As the ANS contributes to the activation of the cardiac system and as a dysfunction of the DA system and the DA D3 receptor is associated with an increased prevalence of hypertension, we next addressed the potential role of DA modulation on the ANS in vivo, and in particular its role in hypertension and with age. Â Â In the first part of this thesis, we provide evidence that DA exerts opposing modulatory effects in ANS-containing segments when compared to segments void of ANS innervation and that this switch in DA modulation in the thoracic spinal cord is reversed by gap junction blockers.Â Â In the second part of the study, we show that aging-related increases in blood pressure and cardiac function in control wild-type (WT) animals were accompanied by bradycardia in the oldest animals. Interestingly, young D3 receptor knockout (D3KO) mice displayed blood pressure and heart rate values that were significantly increased over their age-matched WT controls but similar to those of the old WT group. Ultrasound echocardiography revealed aging-related increases in heart ventricle size in WT animals, but no similar changes in D3KO. In contrast, functional analyses revealed that ejection fraction and fractional shortening were compromised in old WT animals and similar to young D3KO mice. Subsequent histological assays demonstrated an aging-related interstitial fibrosis that peaked in old WT and that was similar to old WT in young D3KO mice.Â Â Taken together, our data suggest that DA-mediated neuromodulatory actions of spinal cord circuits are dependent on the underlying spinal circuitry, and they suggest that a dysfunction of the D3 receptor pathway is sufficient to mimic the increased hypertension and cardiac remodeling observed in the aging heart.Â Â Advisors/Committee Members: Clemens, Stefan (advisor).

Subjects/Keywords: Neuroscience; Physiology; Autonomic nervous system; Dopamine; Hypertension; Spinal cord; Spinal reflex; Biology, Neuroscience; Biology, Physiology; Central Nervous System; Dopamine – physiology; Mice; Receptors, Dopamine D2

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APA (6^th Edition):

Johnson, T. L. (2012). Dopaminergic modulation of the autonomic nervous system: in vitro and in vivo evidence from the mouse. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/4015

Chicago Manual of Style (16^th Edition):

Johnson, Tracy L. “Dopaminergic modulation of the autonomic nervous system: in vitro and in vivo evidence from the mouse.” 2012. Masters Thesis, East Carolina University. Accessed March 05, 2021. http://hdl.handle.net/10342/4015.

MLA Handbook (7^th Edition):

Johnson, Tracy L. “Dopaminergic modulation of the autonomic nervous system: in vitro and in vivo evidence from the mouse.” 2012. Web. 05 Mar 2021.

Vancouver:

Johnson TL. Dopaminergic modulation of the autonomic nervous system: in vitro and in vivo evidence from the mouse. [Internet] [Masters thesis]. East Carolina University; 2012. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10342/4015.

Council of Science Editors:

Johnson TL. Dopaminergic modulation of the autonomic nervous system: in vitro and in vivo evidence from the mouse. [Masters Thesis]. East Carolina University; 2012. Available from: http://hdl.handle.net/10342/4015

9. Kekesi, Orsolya. The effect of chronic and acute inflammatory processes on the electrophysiological properties of the basal forebrain cholinergic system, and the interaction between neuronal and glial cell types.

Degree: 2018, Western Sydney University

URL: http://hdl.handle.net/1959.7/uws:51671

► Ageing and age-related dementias influence every society throughout the world. According to the Australian Bureau of statistics, Dementia is the second leading cause of death… (more)

▼ Ageing and age-related dementias influence every society throughout the world. According to the Australian Bureau of statistics, Dementia is the second leading cause of death of Australians. Dementia is usually referred as a decline in mental ability, inevitably related to loss in cognitive function. Alzheimer’s disease (AD), a neurodegenerative disorder characterized by serious impairment in cognitive function and memory, is the most common form of age-related dementia. Several theories exist regarding the etiology of AD. The cholinergic hypothesis is one of the earliest, claiming that the loss of cholinergic neurons in the basal forebrain and the associated loss of cholinergic innervation play a key role in the onset of the disease. However, recent findings suggest that neuroinflammation is a preliminary process, which plays a role in the onset of Alzheimer’s disease. The aim of this thesis was to investigate the impact of acute and chronic neuroinflammation on the electrophysiological and anatomical properties of cholinergic and GABAergic neurons in the medial septum during ageing, in three different age groups corresponding to young (4-6 months), adult (9-12 months) and aged (>18 months) animals. The first experimental chapter focused on the impact of normal ageing on the medial septal cholinergic system. Whole cell patch clamp electrophysiological recordings indicated on changes in the intrinsic excitability of both cholinergic and GABAergic neurons during ageing, however, it seems like ageing had a greater impact on cholinergic neurons, supporting the idea of their selective vulnerability during neurodegenerative diseases, such AD. A key finding was that medial septal cholinergic neurons have a biphasic characteristic throughout ageing, as they become more excitable in the ‘adult’ age group, but their intrinsic excitability drops in the ‘aged’ group. In the second experimental chapter, we have investigated the impact of acute neuroinflammation on the medial septal cholinergic system and its downstream processes involving cholinergic modulation, such as LTP, in three different age groups. We found that acute neuroinflammation had a differential impact across the different age groups, as it led to an increase in the intrinsic excitability of both young and adult groups, with little effect on neurons from the xiv aged group, abolishing the biphasic alterations in intrinsic excitability seen during ageing. Moreover, extracellular field recordings showed that these alterations affected downstream processes involving cholinergic modulation, such as synaptic plasticity paradigms in the hippocampus. The impact of chronic neuroinflammation was discussed in the third experimental chapter. We investigated the influence of long-term neuroinflammation on the intrinsic properties of GABAergic neurons, as well as synaptic plasticity in the hippocampus during ageing. Our results suggest that chronic neuroinflammation decrease the excitability of GABAergic neurons, and thus increased the overall excitability of the medial… Advisors/Committee Members: Western Sydney University. School of Medicine (Host institution).

Subjects/Keywords: Thesis (Ph.D.) – Western Sydney University, 2018; neurons; physiology; inflammation; age factors; central nervous system; degeneration; immunological aspects; cholinergic mechanisms

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APA (6^th Edition):

Kekesi, O. (2018). The effect of chronic and acute inflammatory processes on the electrophysiological properties of the basal forebrain cholinergic system, and the interaction between neuronal and glial cell types. (Thesis). Western Sydney University. Retrieved from http://hdl.handle.net/1959.7/uws:51671

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kekesi, Orsolya. “The effect of chronic and acute inflammatory processes on the electrophysiological properties of the basal forebrain cholinergic system, and the interaction between neuronal and glial cell types.” 2018. Thesis, Western Sydney University. Accessed March 05, 2021. http://hdl.handle.net/1959.7/uws:51671.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kekesi, Orsolya. “The effect of chronic and acute inflammatory processes on the electrophysiological properties of the basal forebrain cholinergic system, and the interaction between neuronal and glial cell types.” 2018. Web. 05 Mar 2021.

Vancouver:

Kekesi O. The effect of chronic and acute inflammatory processes on the electrophysiological properties of the basal forebrain cholinergic system, and the interaction between neuronal and glial cell types. [Internet] [Thesis]. Western Sydney University; 2018. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1959.7/uws:51671.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kekesi O. The effect of chronic and acute inflammatory processes on the electrophysiological properties of the basal forebrain cholinergic system, and the interaction between neuronal and glial cell types. [Thesis]. Western Sydney University; 2018. Available from: http://hdl.handle.net/1959.7/uws:51671

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

10. Durnin, Leonie. Mechanisms of release, metabolism and action of purines in the enteric and central nervous systems.

Degree: 2013, University of Nevada – Reno

URL: http://hdl.handle.net/11714/3121

► It has been fifty years since the first descriptions of non-adrenergic non-cholinergic (NANC) neurotransmission were made in the gastrointestinal (GI) tract and more than forty… (more)

▼ It has been fifty years since the first descriptions of non-adrenergic non-cholinergic (NANC) neurotransmission were made in the gastrointestinal (GI) tract and more than forty years since it was discovered that NANC neurotransmission was mediated by a purine nucleotide. These influential advances in understanding neuroeffector mechanisms in smooth muscle led Dr. Geoffrey Burnstock to coin the terms `purinergic co-transmission' and `purinergic nerves'. This led to an explosion of interest in purinergic mechanisms controlling the activity of various smooth muscle organs. While adenosine 5'-triphosphate (ATP) has traditionally been considered to be the purine nucleotide responsible for NANC responses, the last decade has uncovered important additional purinergic mechanisms controlling smooth muscle function. Based on the results obtained using extremely sensitive high-pressure liquid chromatography (HPLC) methodologies, nicotinamide adenine dinucleotide (NAD+) has emerged as a novel extracellular signaling factor released during stimulation of peripheral nerves and has a putative neurotransmitter or neuromodulator role. These original findings have significantly advanced our understanding in the field of purinergic signaling.There is substantial evidence that nerve stimulation-evoked release of NAD+ in smooth muscles originates from neural sources, however the complex organization of smooth muscle organs makes verification of vesicular NAD+ release a challenging task. Thus in Chapter 2 of this dissertation we utilized a single cell model to examine storage and release of NAD+ from vesicles in nerve-growth factor (NGF)-differentiated rat pheochromocytoma PC12 cells which phenotypically resemble sympathetic neurons. In this study we verified the presence of NAD+ in vesicles along with ATP and catecholamines (dopamine). Interestingly, we revealed differential mechanisms of release of these three substances from vesicles: release of NAD+ and dopamine required intact SNAP-25-mediated exocytosis whereas ATP was released largely via SNAP-25-independent mechanisms. These observations in conjunction with a previous finding demonstrating ω-conotoxin GVIA-insensitive ATP release in blood vessels led us to question the true identity of the NANC neurotransmitter in GI muscles where purinergic neurotransmission was first described.In the GI tract, purines released from inhibitory motor neurons elicit postsynaptic hyperpolarization transients (inhibitory junction potentials, IJPs) in circular smooth muscles causing relaxation. In the attempt to clarify which purines are involved in mediating gut relaxation we carried out a series of experiments in murine and primate colonic muscles comparing mechanisms of release, metabolism and action of extracellular purines. In Chapter 3 we demonstrated that electrical field stimulation (EFS) evoked release of NAD+ that was dependent on the level of nerve stimulation and was significantly attenuated by blockers of neural activity. We also demonstrated that postsynaptic hyperpolarizations to… Advisors/Committee Members: Mutafova-Yambolieva, Violeta N (advisor), Sanders, Kenton M (committee member), Ward, Sean M (committee member), Perrino, Brian A (committee member), Kidd, Thomas (committee member).

Subjects/Keywords: ATP; Central nervous system; Colon; Enteric nervous system; NAD; Purinergic neurotransmission

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Durnin, L. (2013). Mechanisms of release, metabolism and action of purines in the enteric and central nervous systems. (Thesis). University of Nevada – Reno. Retrieved from http://hdl.handle.net/11714/3121

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Durnin, Leonie. “Mechanisms of release, metabolism and action of purines in the enteric and central nervous systems.” 2013. Thesis, University of Nevada – Reno. Accessed March 05, 2021. http://hdl.handle.net/11714/3121.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Durnin, Leonie. “Mechanisms of release, metabolism and action of purines in the enteric and central nervous systems.” 2013. Web. 05 Mar 2021.

Vancouver:

Durnin L. Mechanisms of release, metabolism and action of purines in the enteric and central nervous systems. [Internet] [Thesis]. University of Nevada – Reno; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/11714/3121.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Durnin L. Mechanisms of release, metabolism and action of purines in the enteric and central nervous systems. [Thesis]. University of Nevada – Reno; 2013. Available from: http://hdl.handle.net/11714/3121

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Utah

11. Weakly, James Neal. Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission.

Degree: PhD, Pharmacology & Toxicology;, 1968, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/514/rec/95

► The mechanism of the depression of central nervous functions produced by anesthetic agents has been of interest to physiologists, pharmacologist, and physicians for some time.… (more)

▼ The mechanism of the depression of central nervous functions produced by anesthetic agents has been of interest to physiologists, pharmacologist, and physicians for some time. Despite the widespread use of central nervous system depressant, relatively little is known about their effects on nervous tissue at the cellular level, particularly their actions on presynaptic nerve terminals. The present investigation attempts to analyze the effects of three central nervous system depressants, thiopental, pentobarbital, and ether, with the use of the technique of intracellular recording. The monosynaptic pathway in the spinal cord of the cat was selected as the model to be used in this investigation. This selection was made on the basis of the abundance of knowledge that has been accumulated in the past 25 years regarding the physiology of this central pathway, and because the drugs employed in this investigation has been shown to exert effects on the spinal cord by various Neurophysiological and neuro-pharmacological techniques other than intracellular recording. In order to examine the effects of these anesthetics on the presynaptic mechanism(s) responsible for transmitter release, advantage was taken of the fact that transmission of excitation of the spinal monosynaptic pathway is quantal in nature, i.e., transmitter is released as multi-molecular packages of quanta in a manner similar to the transmitter at the neuromuscular junction. In the doses employed, the drugs were observed to block reflex transmission in the monosynaptic pathway. The barbiturates were found to be without effects on parameters attributable to the postsynaptic membrane, i.e., input resistance of the motoneurons membrane, strength-duration relations for the motoneurons, and sensitivity of the subsynaptic membrane to the effects of the transmitter. Thiopental and pentobarbital reduced the amount of transmitter released by a single afferent impulse from a Group la fiber in the muscle nerve. The observed magnitude to the reduction in transmitter release is adequate to explain the reduction in reflex transmission through the pathway. It is concluded that the actions of thiopental and pentobarbital, in the doses employed, are confined to presynaptic nerve terminals and that the depression of reflex transmission in the spinal monosynaptic pathway is the result of a decrease in the statistical probability of transmitter release. Ether also decreased the amount of transmitter released by single afferent impulses, but this does not appear to be the sole factor responsible for the observed decreased in monosynaptic reflex transmission produced by this agent.

Subjects/Keywords: Central Nervous System

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Weakly, J. N. (1968). Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/514/rec/95

Chicago Manual of Style (16^th Edition):

Weakly, James Neal. “Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission.” 1968. Doctoral Dissertation, University of Utah. Accessed March 05, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/514/rec/95.

MLA Handbook (7^th Edition):

Weakly, James Neal. “Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission.” 1968. Web. 05 Mar 2021.

Vancouver:

Weakly JN. Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission. [Internet] [Doctoral dissertation]. University of Utah; 1968. [cited 2021 Mar 05]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/514/rec/95.

Council of Science Editors:

Weakly JN. Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission. [Doctoral Dissertation]. University of Utah; 1968. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/514/rec/95

University of Alberta

12. Lagerquist, Olle. Neuromuscular electrical stimulation and the central nervous system.

Degree: PhD, Center for Neuroscience and the Faculty of Physical Education and Recreation, 2009, University of Alberta

URL: https://era.library.ualberta.ca/files/1831ck60w

► Neuromuscular electrical stimulation (NMES) is a common therapeutic tool for persons with movement disorders. The manner in which NMES generates muscular contractions has traditionally been… (more)

▼ Neuromuscular electrical stimulation (NMES) is a common therapeutic tool for persons with movement disorders. The manner in which NMES generates muscular contractions has traditionally been attributed to the depolarization of motor axons underneath the stimulating electrodes, a purely peripheral mechanism, which does not involve the central nervous system (CNS). During NMES however, sensory axons are also recruited, initiating an afferent volley which can affect both spinal and cortical centers. This thesis is focused on identifying how this afferent volley influences NMES-evoked contractions and CNS excitability. Four projects are described in which NMES was delivered to generate plantar-flexion contractions. The first goal was to establish the influence of stimulus pulse width on the central recruitment of motoneurons. Contrary to previous findings, changing the pulse width did not significantly alter maximal soleus H-reflex amplitudes; however, wider pulses resulted in a leftward shift of the H-reflex recruitment curve and increased H-reflex amplitudes on the ascending limb of the recruitment curve. The second goal was to examine the effect of stimulus pulse-width on electromyograpic responses and torque during NMES. During 20 Hz NMES, wide pulse widths depressed motor-waves (M-waves) and enhanced H-reflexes, generating larger contractions with a relatively greater central contribution, than when narrow pulses were used. The third project compared the torque produced during NMES-evoked contractions before and during a complete anesthetic block of the tibial and common peroneal nerves. Results from this project showed that contractions arising from a combination of central and peripheral mechanisms fatigue less than contractions that develop from the recruitment of motor axons alone. The final project investigated how spinal and corticospinal excitability associated with the soleus muscles are affected following NMES, voluntary contractions, or a combination of both. It was found that a combination of voluntary contractions and electrical stimulation induced plastic changes in the spinal circuitry of the stimulated muscle without affecting cortical circuitry or inducing any contralateral effects. Collectively, these experiments highlight that wider pulse widths induce a greater reflexive recruitment of motoneurons which contributes to the evoked torque during NMES, and that the evoked afferent volley reduces fatigue and influences spinal circuitry plasticity in the plantar-flexors. Methods to enhance the afferent volley during NMES are only beginning to be tested in clinical populations and future experiments will determine the potential efficacy for persons with movement disorders.

Subjects/Keywords: central nervous system; neuromuscular electrical stimulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lagerquist, O. (2009). Neuromuscular electrical stimulation and the central nervous system. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/1831ck60w

Chicago Manual of Style (16^th Edition):

Lagerquist, Olle. “Neuromuscular electrical stimulation and the central nervous system.” 2009. Doctoral Dissertation, University of Alberta. Accessed March 05, 2021. https://era.library.ualberta.ca/files/1831ck60w.

MLA Handbook (7^th Edition):

Lagerquist, Olle. “Neuromuscular electrical stimulation and the central nervous system.” 2009. Web. 05 Mar 2021.

Vancouver:

Lagerquist O. Neuromuscular electrical stimulation and the central nervous system. [Internet] [Doctoral dissertation]. University of Alberta; 2009. [cited 2021 Mar 05]. Available from: https://era.library.ualberta.ca/files/1831ck60w.

Council of Science Editors:

Lagerquist O. Neuromuscular electrical stimulation and the central nervous system. [Doctoral Dissertation]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/1831ck60w

Universiteit Utrecht

13. Lam, J.C. Functional parameters for the development of the central nervous system of piglets.

Degree: 2016, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/330679

► Because of improved health care the survival rate of preterm infants and low birth weight infants is increased. These infants often have brain abnormalities resulting… (more)

Subjects/Keywords: central nervous system; piglets; test battery; development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lam, J. C. (2016). Functional parameters for the development of the central nervous system of piglets. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/330679

Chicago Manual of Style (16^th Edition):

Lam, J C. “Functional parameters for the development of the central nervous system of piglets.” 2016. Masters Thesis, Universiteit Utrecht. Accessed March 05, 2021. http://dspace.library.uu.nl:8080/handle/1874/330679.

MLA Handbook (7^th Edition):

Lam, J C. “Functional parameters for the development of the central nervous system of piglets.” 2016. Web. 05 Mar 2021.

Vancouver:

Lam JC. Functional parameters for the development of the central nervous system of piglets. [Internet] [Masters thesis]. Universiteit Utrecht; 2016. [cited 2021 Mar 05]. Available from: http://dspace.library.uu.nl:8080/handle/1874/330679.

Council of Science Editors:

Lam JC. Functional parameters for the development of the central nervous system of piglets. [Masters Thesis]. Universiteit Utrecht; 2016. Available from: http://dspace.library.uu.nl:8080/handle/1874/330679

Texas A&M University

14. Whitener, Amy Elizabeth. The Role of Wnt Signaling in Temporal Patterning and Cell Fate Specification of the Midbrain Hindbrain Domain.

Degree: PhD, Biology, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/161629

► The Midbrain Hindbrain Domain (MHD) is a region of the central nervous system consisting of the midbrain, midbrain hindbrain boundary (MHB) and anterior hindbrain. The… (more)

▼ The Midbrain Hindbrain Domain (MHD) is a region of the central nervous system consisting of the midbrain, midbrain hindbrain boundary (MHB) and anterior hindbrain. The MHB is an organizer that patterns the midbrain and anterior hindbrain. It is important to understand how organizers such as the MHB are formed to better understand how the vertebrate brain is patterned and develops. I have examined how timing of signaling by the canonical Wnt/β -catenin signaling pathway affects MHD specification and patterning by inhibiting Wnt signaling at specific developmental time intervals and analyzing the resulting phenotypes by morphological analysis and in situ hybridization. Four Wnt genes, wnt1, wnt10b, wnt3, and wnt3a, have overlapping expression patterns in the MHD, but their relative roles in MHB development are unclear. wnt3a, wnt1, and wnt10b are activated earlier in development than wnt3. wnt3a, wnt1, and wnt10b have been shown to work in combination to regulate MHB development which lead to the question what is the role of wnt3 in this process. I specifically examined the role of wnt3 during MHB development by knocking down wnt3 in combination with the other three Wnt genes and performed in situ hybridizations using anterior and posterior neural markers. We observed that after inhibition of Wnt signaling at early developmental time intervals, midbrain and anterior hindbrain formation is disrupted but not MHB development. When Wnt signaling is blocked at later developmental time intervals, MHD patterning and formation are disrupted. Our data show forebrain fates expand posteriorly and midbrain and anterior hindbrain fates are reduced at later developmental stages. These data suggest Wnt signaling represses anterior neural fates and advances posterior neural fates in MHD patterning and specification. When wnt3 is inhibited in combination with wnt1 and wnt10b, I observed that the MHB is partially reduced, whereas the MHB is absent when wnt3 and wnt3a in combination with wnt1 and wnt10b are inhibited. When wnt3 and wnt3a are blocked, the MHB is absent. These data suggest that these Wnt genes work in combination to regulate MHB formation but have differential requirements in this process. In conclusion, our results suggest Wnt signaling represses forebrain fates, while promoting midbrain, MHB, and anterior hindbrain. Also, multiple Wnt genes expressed in the MHB regulate MHB formation, but their functions are different. Advisors/Committee Members: Lekven, Arne C (advisor), Carney, Ginger E (committee member), Gumienny, Tina L (committee member), Kunkel, Gary R (committee member).

Subjects/Keywords: Zebrafish; Central Nervous System; Embryonic Development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Whitener, A. E. (2017). The Role of Wnt Signaling in Temporal Patterning and Cell Fate Specification of the Midbrain Hindbrain Domain. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/161629

Chicago Manual of Style (16^th Edition):

Whitener, Amy Elizabeth. “The Role of Wnt Signaling in Temporal Patterning and Cell Fate Specification of the Midbrain Hindbrain Domain.” 2017. Doctoral Dissertation, Texas A&M University. Accessed March 05, 2021. http://hdl.handle.net/1969.1/161629.

MLA Handbook (7^th Edition):

Whitener, Amy Elizabeth. “The Role of Wnt Signaling in Temporal Patterning and Cell Fate Specification of the Midbrain Hindbrain Domain.” 2017. Web. 05 Mar 2021.

Vancouver:

Whitener AE. The Role of Wnt Signaling in Temporal Patterning and Cell Fate Specification of the Midbrain Hindbrain Domain. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1969.1/161629.

Council of Science Editors:

Whitener AE. The Role of Wnt Signaling in Temporal Patterning and Cell Fate Specification of the Midbrain Hindbrain Domain. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/161629

University of Texas Southwestern Medical Center

15. Meredith, David Miles. Regulation and Function of PTF1a in the Developing Nervous System.

Degree: 2012, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1110

► Basic helix-loop-helix transcription factors serve many roles in development, including regulation of neurogenesis. Many of these factors are activated in naive neural progenitors and function… (more)

▼ Basic helix-loop-helix transcription factors serve many roles in development, including regulation of neurogenesis. Many of these factors are activated in naive neural progenitors and function to promote neuronal differentiation and cell-type specification. Ptf1a is a basic helix-loop-helix protein that is required for proper inhibitory neuron formation in several regions of the developing nervous system, including the spinal cord, cerebellum, retina, and hypothalamus. In addition, Ptf1a is essential for proper pancreas formation and exocrine function. In both the nervous system and pancreas, Ptf1a functions as a switch in cell fate determination. In the absence of Ptf1a, inhibitory neurons are lost and those cells instead adopt an excitatory identity. Similarly, endodermal progenitors will assume duodenal characteristics in place of a pancreatic identity when Ptf1a is lost. Like most other tissue-specific basic-helix-loop-helix factors, Ptf1a dimerizes with E-proteins and binds a degenerate hexameric E-box motif (CANNTG). Ptf1a is unique, however, in that it also requires the presence of Rbpj(l) to form an active transcription complex, PTF1. This interaction is central to Ptf1a function, as disruption of Ptf1a?s ability to bind Rbpj in vivo phenocopies the Ptf1a null in the nervous system and pancreas. Similarly, all targets described thus far for Ptf1a require an intact PTF1 binding site, which includes both an E-box and Rbpj binding site. In order to understand how a factor such as Ptf1a is capable of giving rise to such disparate organs, I wanted to place it in context of a larger regulatory network that directs a multipotent progenitor into a mature inhibitory neuron. Thus, I examine two regulatory schemes controlling Ptf1a expression during development in Chapters two and three. I then investigate direct Ptf1a targets in a genome-wide fashion using massively parallel sequencing technology in Chapters four and five. These efforts uncovered that Ptf1a employs several mechanisms to achieve proper cell-type specification, including initiation of transcription factor cascades, direct activation of inhibitory neuron machinery, and direct suppression of the excitatory neuron program. Furthermore, I identify novel binding modes and potential co-regulatory factors that could impart tissue-specific function. Advisors/Committee Members: Johnson, Jane E..

Subjects/Keywords: Central Nervous System; Transcription Factors; Neurogenesis

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APA (6^th Edition):

Meredith, D. M. (2012). Regulation and Function of PTF1a in the Developing Nervous System. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1110

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Meredith, David Miles. “Regulation and Function of PTF1a in the Developing Nervous System.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed March 05, 2021. http://hdl.handle.net/2152.5/1110.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Meredith, David Miles. “Regulation and Function of PTF1a in the Developing Nervous System.” 2012. Web. 05 Mar 2021.

Vancouver:

Meredith DM. Regulation and Function of PTF1a in the Developing Nervous System. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2152.5/1110.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Meredith DM. Regulation and Function of PTF1a in the Developing Nervous System. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1110

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Adelaide

16. Rogers, Nicholas Alan. Expression and functional analysis of SOX3 in murine neurogenesis.

Degree: 2014, University of Adelaide

URL: http://hdl.handle.net/2440/92331

► The Sox (SRY-related HMG box) family of proteins are transcription factors. There are, in total, 30 different genes in the Sox family. Each Sox protein… (more)

▼ The Sox (SRY-related HMG box) family of proteins are transcription factors. There are, in total, 30 different genes in the Sox family. Each Sox protein contains a HMG box (high-mobility-group) which functions as a DNA binding domain. The HMG box is highly conserved (>50% identity) throughout the entire Sox family. Sox3 belongs to the SoxB1 subgroup. SOX3 has been associated with human CNS related disorders. Duplication and mutations of SOX3 have been identified in patients with X-linked hypopituitarism (XH). Afflicted XH patients suffer from varying levels of mental retardation and pituitary hormone deficiencies which can lead to short stature. Previous studies have shown that Sox3 is expressed in nascent neuroprogenitor cells and is functionally required in mammals for development of the dorsal telencephalon and hypothalamus. Using a SOX3-specific antibody, data within my thesis shows that murine SOX3 expression is maintained throughout telencephalic neurogenesis and is restricted to progenitor cells with neuroepithelial and radial glial morphologies. In addition, characterisation of SOX3 expression within the adult neurogenic regions indicates that it is a lifelong marker of neuroprogenitor cells. In contrast to the telencephalon, Sox3 expression within the developing hypothalamus is up-regulated in developing neurons and is maintained in a subset of differentiated hypothalamic cells through to adulthood. In addition, using genome wide expression analysis examining a Sox3 null neural progenitor population, I identified a number of putative Sox3 targets. The data identified Dbx1 as a robust Sox3 target with Dbx1 down-regulation, at both the mRNA and Protein level, within Sox3 null mice at early stages of CNS development. I also independently confirm a number of SOX3 binding sites surrounding Dbx1, with one site showing clear enrichment in vivo. In addition, correlation between these putative targets and that of a previously published SOX3-ChIP data set show a clear enrichment for SOXB1 binding sites near the mis-regulated genes suggesting they are direct targets of Sox3. Taken together, data presented within my thesis identifies new regions of Sox3 expression and putative Sox3 targets. This data helps advance our knowledge of Sox3 regulation and function within CNS development. Advisors/Committee Members: Thomas, Paul Quinton (advisor), School of Molecular and Biomedical Science (school).

Subjects/Keywords: Sox3; neurogenesis; central nervous system; neural progenitor

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APA (6^th Edition):

Rogers, N. A. (2014). Expression and functional analysis of SOX3 in murine neurogenesis. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/92331

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rogers, Nicholas Alan. “Expression and functional analysis of SOX3 in murine neurogenesis.” 2014. Thesis, University of Adelaide. Accessed March 05, 2021. http://hdl.handle.net/2440/92331.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rogers, Nicholas Alan. “Expression and functional analysis of SOX3 in murine neurogenesis.” 2014. Web. 05 Mar 2021.

Vancouver:

Rogers NA. Expression and functional analysis of SOX3 in murine neurogenesis. [Internet] [Thesis]. University of Adelaide; 2014. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2440/92331.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rogers NA. Expression and functional analysis of SOX3 in murine neurogenesis. [Thesis]. University of Adelaide; 2014. Available from: http://hdl.handle.net/2440/92331

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Columbia University

17. Aber, Etan. Myelin is remodeled cell-autonomously by oligodendroglial macroautophagy.

Degree: 2018, Columbia University

URL: https://doi.org/10.7916/D8V99M16

► Myelination of axons in the CNS by oligodendrocytes (OLs) is critical for the rapid and reliable conduction of action potentials down neuronal axons, as evidenced… (more)

▼ Myelination of axons in the CNS by oligodendrocytes (OLs) is critical for the rapid and reliable conduction of action potentials down neuronal axons, as evidenced by the severe disabilities associated with myelin loss in multiple sclerosis and other diseases of myelin. The specification, differentiation, and maturation of OLs along with myelin formation by OLs have been thoroughly characterized. How myelin is turned over, however remains unclear. It is unsurprising that little is known about myelin turnover considering that for decades following their discovery, myelin and OLs were considered static elements in the adult nervous system. Recent evidence, however, shows that myelin in the CNS is actually plastic. Moreover, myelin remodeling in humans has been suggested to be mediated by mature OLs. As mature OLs have limited capacity to generate new myelin sheaths, we must ask whether mature OLs can remodel the myelin at preexisting myelin sheaths. One intriguing but unproven possibility is that myelin at individual internodes may be remodeled cell-autonomously by mature OLs to modulate neuronal circuit function. Macroautophagy (MA) is responsible for the lysosome-mediated elimination of cytosolic proteins, lipids, and organelles. MA achieves this by capturing cargo in bulk or selectively in a transient, multilamellar structure known as an autophagosome (AP). In this study, we used a combination of in vivo and cellular approaches to test the hypothesis that MA in OLs may be important for myelin remodeling in the adult CNS. We establish that myelin of individual internodes is remodeled, and does so through the coordinated efforts of endocytosis and MA. We found that autophagy protein Atg7 is essential for myelin remodeling in vivo: loss of Atg7 in OLs leads to an age-dependent increase of myelin at the internode and the formation of aberrant myelin structures, most notably myelin outfoldings. In addition, we find that MA has the potential to occur throughout the mature OL, and examination of OLs in culture suggests that formation of a mature AP structure, the amphisome, is required to facilitate the efficient degradation of myelin-containing endocytic structures. Together, we propose that myelin is a dynamic structure that is regularly remodeled through the cooperative efforts of MA and endocytosis. These findings raise the possibility that myelin remodeling is involved in neural plasticity and the tuning of neural circuits.

Subjects/Keywords: Neurosciences; Cytology; Myelination; Central nervous system

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APA (6^th Edition):

Aber, E. (2018). Myelin is remodeled cell-autonomously by oligodendroglial macroautophagy. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8V99M16

Chicago Manual of Style (16^th Edition):

Aber, Etan. “Myelin is remodeled cell-autonomously by oligodendroglial macroautophagy.” 2018. Doctoral Dissertation, Columbia University. Accessed March 05, 2021. https://doi.org/10.7916/D8V99M16.

MLA Handbook (7^th Edition):

Aber, Etan. “Myelin is remodeled cell-autonomously by oligodendroglial macroautophagy.” 2018. Web. 05 Mar 2021.

Vancouver:

Aber E. Myelin is remodeled cell-autonomously by oligodendroglial macroautophagy. [Internet] [Doctoral dissertation]. Columbia University; 2018. [cited 2021 Mar 05]. Available from: https://doi.org/10.7916/D8V99M16.

Council of Science Editors:

Aber E. Myelin is remodeled cell-autonomously by oligodendroglial macroautophagy. [Doctoral Dissertation]. Columbia University; 2018. Available from: https://doi.org/10.7916/D8V99M16

Hong Kong University of Science and Technology

18. Ding, Yue LIFS. Mammalian target of rapamycin is required for axon growth of adult dorsal root ganglion neurons.

Degree: 2015, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-97094 ; https://doi.org/10.14711/thesis-b1585232 ; http://repository.ust.hk/ir/bitstream/1783.1-97094/1/th_redirect.html

► Different from neurons in the central nervous system, adult neurons in the mammalian peripheral nervous system can regenerate axons after injury partially by enhancing the… (more)

Subjects/Keywords: Rapamycin ; Axons ; Central nervous system ; Growth

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APA (6^th Edition):

Ding, Y. L. (2015). Mammalian target of rapamycin is required for axon growth of adult dorsal root ganglion neurons. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-97094 ; https://doi.org/10.14711/thesis-b1585232 ; http://repository.ust.hk/ir/bitstream/1783.1-97094/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ding, Yue LIFS. “Mammalian target of rapamycin is required for axon growth of adult dorsal root ganglion neurons.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed March 05, 2021. http://repository.ust.hk/ir/Record/1783.1-97094 ; https://doi.org/10.14711/thesis-b1585232 ; http://repository.ust.hk/ir/bitstream/1783.1-97094/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ding, Yue LIFS. “Mammalian target of rapamycin is required for axon growth of adult dorsal root ganglion neurons.” 2015. Web. 05 Mar 2021.

Vancouver:

Ding YL. Mammalian target of rapamycin is required for axon growth of adult dorsal root ganglion neurons. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2021 Mar 05]. Available from: http://repository.ust.hk/ir/Record/1783.1-97094 ; https://doi.org/10.14711/thesis-b1585232 ; http://repository.ust.hk/ir/bitstream/1783.1-97094/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ding YL. Mammalian target of rapamycin is required for axon growth of adult dorsal root ganglion neurons. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: http://repository.ust.hk/ir/Record/1783.1-97094 ; https://doi.org/10.14711/thesis-b1585232 ; http://repository.ust.hk/ir/bitstream/1783.1-97094/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universitat Politècnica de València

19. Baiget Orts, María Amparo. HYALURONAN BASED BIOMATERIALS FOR CENTRAL NERVOUS TISSUE REGENERATION .

Degree: 2012, Universitat Politècnica de València

URL: http://hdl.handle.net/10251/14576

► The aim of this Thesis is to investigate the use of hyaluronic acid as a material for the design of scaffolds aimed at CNS regeneration.… (more)

Subjects/Keywords: Angiogenesis; Biomaterials; Hyaluronic acid; Central nervous system

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APA (6^th Edition):

Baiget Orts, M. A. (2012). HYALURONAN BASED BIOMATERIALS FOR CENTRAL NERVOUS TISSUE REGENERATION . (Doctoral Dissertation). Universitat Politècnica de València. Retrieved from http://hdl.handle.net/10251/14576

Chicago Manual of Style (16^th Edition):

Baiget Orts, María Amparo. “HYALURONAN BASED BIOMATERIALS FOR CENTRAL NERVOUS TISSUE REGENERATION .” 2012. Doctoral Dissertation, Universitat Politècnica de València. Accessed March 05, 2021. http://hdl.handle.net/10251/14576.

MLA Handbook (7^th Edition):

Baiget Orts, María Amparo. “HYALURONAN BASED BIOMATERIALS FOR CENTRAL NERVOUS TISSUE REGENERATION .” 2012. Web. 05 Mar 2021.

Vancouver:

Baiget Orts MA. HYALURONAN BASED BIOMATERIALS FOR CENTRAL NERVOUS TISSUE REGENERATION . [Internet] [Doctoral dissertation]. Universitat Politècnica de València; 2012. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10251/14576.

Council of Science Editors:

Baiget Orts MA. HYALURONAN BASED BIOMATERIALS FOR CENTRAL NERVOUS TISSUE REGENERATION . [Doctoral Dissertation]. Universitat Politècnica de València; 2012. Available from: http://hdl.handle.net/10251/14576

20. Perez Garnes, Manuel. Structures based on semi-degradable biomaterials for neural regeneration in the central nervous system .

Degree: 2015, Universitat Politècnica de València

URL: http://hdl.handle.net/10251/48799

► Se pretende obtener un material semibiodegradable basado en ácido hialurónico químicamente enlazado a cadenas de polímeros acrílicos. Los hidrogeles de ácido hialurónico presentan en general… (more)

Subjects/Keywords: Hyaluronan; Semi-degradable biomaterials; Central nervous system

11 more images…

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APA (6^th Edition):

Perez Garnes, M. (2015). Structures based on semi-degradable biomaterials for neural regeneration in the central nervous system . (Doctoral Dissertation). Universitat Politècnica de València. Retrieved from http://hdl.handle.net/10251/48799

Chicago Manual of Style (16^th Edition):

Perez Garnes, Manuel. “Structures based on semi-degradable biomaterials for neural regeneration in the central nervous system .” 2015. Doctoral Dissertation, Universitat Politècnica de València. Accessed March 05, 2021. http://hdl.handle.net/10251/48799.

MLA Handbook (7^th Edition):

Perez Garnes, Manuel. “Structures based on semi-degradable biomaterials for neural regeneration in the central nervous system .” 2015. Web. 05 Mar 2021.

Vancouver:

Perez Garnes M. Structures based on semi-degradable biomaterials for neural regeneration in the central nervous system . [Internet] [Doctoral dissertation]. Universitat Politècnica de València; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10251/48799.

Council of Science Editors:

Perez Garnes M. Structures based on semi-degradable biomaterials for neural regeneration in the central nervous system . [Doctoral Dissertation]. Universitat Politècnica de València; 2015. Available from: http://hdl.handle.net/10251/48799

Hong Kong University of Science and Technology

21. Wang, Xuejie LIFS. TSC1 deletion in microglia induces the hypertrophy of the microglia and inhibits axon regeneration.

Degree: 2017, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-105667 ; https://doi.org/10.14711/thesis-991012564268903412 ; http://repository.ust.hk/ir/bitstream/1783.1-105667/1/th_redirect.html

► As the resident immune cells in the central nervous system (CNS), microglia play an important role in maintaining homeostasis during development and in adult. After… (more)

Subjects/Keywords: Microglia ; Central nervous system ; Regeneration ; Cells ; Regulation

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APA (6^th Edition):

Wang, X. L. (2017). TSC1 deletion in microglia induces the hypertrophy of the microglia and inhibits axon regeneration. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-105667 ; https://doi.org/10.14711/thesis-991012564268903412 ; http://repository.ust.hk/ir/bitstream/1783.1-105667/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wang, Xuejie LIFS. “TSC1 deletion in microglia induces the hypertrophy of the microglia and inhibits axon regeneration.” 2017. Thesis, Hong Kong University of Science and Technology. Accessed March 05, 2021. http://repository.ust.hk/ir/Record/1783.1-105667 ; https://doi.org/10.14711/thesis-991012564268903412 ; http://repository.ust.hk/ir/bitstream/1783.1-105667/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wang, Xuejie LIFS. “TSC1 deletion in microglia induces the hypertrophy of the microglia and inhibits axon regeneration.” 2017. Web. 05 Mar 2021.

Vancouver:

Wang XL. TSC1 deletion in microglia induces the hypertrophy of the microglia and inhibits axon regeneration. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2017. [cited 2021 Mar 05]. Available from: http://repository.ust.hk/ir/Record/1783.1-105667 ; https://doi.org/10.14711/thesis-991012564268903412 ; http://repository.ust.hk/ir/bitstream/1783.1-105667/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wang XL. TSC1 deletion in microglia induces the hypertrophy of the microglia and inhibits axon regeneration. [Thesis]. Hong Kong University of Science and Technology; 2017. Available from: http://repository.ust.hk/ir/Record/1783.1-105667 ; https://doi.org/10.14711/thesis-991012564268903412 ; http://repository.ust.hk/ir/bitstream/1783.1-105667/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

22. Trinh, Irene. An In Vivo Screen for Genes Involved in Central Nervous System Control of Obesity Identifies Diacylglycerol Kinase as a Regulator of Insulin Secretion.

Degree: PhD, 2017, University of Toronto

URL: http://hdl.handle.net/1807/97800

►

The increasing prevalence of obesity as well as its association with many chronic diseases has turned obesity into a major health concern worldwide. Obesity has… (more)

▼

The increasing prevalence of obesity as well as its association with many chronic diseases has turned obesity into a major health concern worldwide. Obesity has many underlying environmental and genetic factors that disturb the balance between energy intake and energy expenditure, which is controlled by the central nervous system. The goal of my project is to help further our understanding of these CNS mechanisms by using the powerful tools available in Drosophila melanogaster to identify neuronal genes involved in energy homeostasis. Using the neuronal fru-Gal4 driver we performed an RNAi screen with 1748 genes and assayed for obese or lean phenotypes defined as increases or decreases in triacylglycerol (TAG) levels. After 3 rounds of screening I identified 25 hits that were reproducible and confirmed these phenotypes with independent RNAi lines. One of these hits was Diacylglycerol kinase (Dgk) whose mammalian homologues have been implicated in genome-wide association studies for metabolic defects. Manipulation of neuronal Dgk levels affects TAG and carbohydrate levels but these effects donâ t seem to be mediated through Dgkâ s regulation of DAG, PA levels or PKC activity. I hypothesized that Dgk acts in the insulin-producing cells (IPCs), a set of neurosecretory neurons that secrete Drosophila insulin-like peptides (dILPs) and are involved in the regulation of dILP secretion. Knockdown or overexpression of Dgk within the IPCs reproduces the same TAG, glucose and glycogen phenotypes seen with fru-Gal4. Moreover, overexpression of kinase-dead Dgk, but not wild-type, decreased circulating dILP2 and dILP5 levels resulting in lower insulin signalling activity. Conversely, despite having higher circulating dILP levels, Dgk RNAi flies have decreased pathway activity suggesting that they are insulin-resistant. Thus, after screening over 1700 genes in vivo I identified 25 genes as potential neuronal mediators of energy homeostasis. My results have also shown that one of these genes, Dgk, acts within the insulin-producing cells to regulate the secretion of dILPs and energy homeostasis in Drosophila.

2019-11-17 00:00:00

Advisors/Committee Members: Boulianne, Gabrielle L, Molecular and Medical Genetics.

Subjects/Keywords: Central Nervous System; Diacylglycerol kinase; Obesity; 0369

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Trinh, I. (2017). An In Vivo Screen for Genes Involved in Central Nervous System Control of Obesity Identifies Diacylglycerol Kinase as a Regulator of Insulin Secretion. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/97800

Chicago Manual of Style (16^th Edition):

Trinh, Irene. “An In Vivo Screen for Genes Involved in Central Nervous System Control of Obesity Identifies Diacylglycerol Kinase as a Regulator of Insulin Secretion.” 2017. Doctoral Dissertation, University of Toronto. Accessed March 05, 2021. http://hdl.handle.net/1807/97800.

MLA Handbook (7^th Edition):

Trinh, Irene. “An In Vivo Screen for Genes Involved in Central Nervous System Control of Obesity Identifies Diacylglycerol Kinase as a Regulator of Insulin Secretion.” 2017. Web. 05 Mar 2021.

Vancouver:

Trinh I. An In Vivo Screen for Genes Involved in Central Nervous System Control of Obesity Identifies Diacylglycerol Kinase as a Regulator of Insulin Secretion. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1807/97800.

Council of Science Editors:

Trinh I. An In Vivo Screen for Genes Involved in Central Nervous System Control of Obesity Identifies Diacylglycerol Kinase as a Regulator of Insulin Secretion. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/97800

University of Melbourne

23. Hay, Curtis Mackenzie. Investigating the role of Gpr62 in oligodendrocyte development and central nervous system myelination.

Degree: 2015, University of Melbourne

URL: http://hdl.handle.net/11343/58589

► Myelination is a highly regulated process in the vertebrate nervous system whereby glial cells wraps axons with insulating myelin in order to allow rapid electrical… (more)

▼ Myelination is a highly regulated process in the vertebrate nervous system whereby glial cells wraps axons with insulating myelin in order to allow rapid electrical conduction and metabolic support, a process which is fundamental for proper axon function and survival. Current research in the central nervous system (CNS) has focused on factors affecting oligodendroglial differentiation, yet the molecular interactions that occur post-differentiation between the oligodendrocyte and other CNS cell types during developmental myelination and myelin maintenance are still unclear. This thesis investigates the role the orphan G-protein coupled receptor (GPCR) Gpr62, as it relates to oligodendrocyte development and myelination. First, in silico analysis in conjunction with in situ hybridization showed that Gpr62 is specific to and highly expressed in the CNS, specifically within myelinating oligodendrocytes. Moreover, Gpr62 expression was shown to be regulated by myelin regulatory factor (MyRF), a key transcription factor regulating expression of major myelin genes. Secondly, a germline knockout mouse strain of Gpr62 was investigated. Gpr62 knockout mice showed no significant affect on myelin thickness, myelin gene or protein expression, initiation of myelination, or oligodendrocyte formation relative to their wildtype littermates, all of which were assessed in the developing, adult, and aging brain. An RNA-sequencing analysis revealed few differentially expressed genes between the knockout and wildtype controls, which were not validated in independent cohorts. Interestingly, the RNA- sequencing revealed several differentially expressed genes in close proximity to the Gpr62 locus. Further analysis indicated that these differentially regulated genes proximal to the Gpr62 locus were the result of Sv129-inherited DNA from the ES cells used for targeting, a result with significant implications for other germline knockout lines generated in the same fashion. Finally, forced viral expression of a tagged version of Gpr62 using an AAV virus demonstrated for the first time the cellular localization of the Gpr62 protein, showing expression within the oligodendrocyte extensions and myelin sheath, expressed along the adaxonal space. Collectively, these results indicated that Gpr62 is a novel oligodendrocyte-specific GPCR located along the myelin sheath, yet it is dispensable for myelin development and maintenance. Thus, failure to identify a role for Gpr62 may be the results Gpr62 having a function in the oligodendrocyte outside of developmental myelination. Indeed, the specificity and regulation of Gpr62 expression in oligodendrocytes by MyRF, and its localization within the myelin sheath, suggests Gpr62 may play a role in the oligodendrocyte that has yet to be explored.

Subjects/Keywords: oligodendrocyte; myelination; myelin; central nervous system; Gpr62

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APA (6^th Edition):

Hay, C. M. (2015). Investigating the role of Gpr62 in oligodendrocyte development and central nervous system myelination. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/58589

Chicago Manual of Style (16^th Edition):

Hay, Curtis Mackenzie. “Investigating the role of Gpr62 in oligodendrocyte development and central nervous system myelination.” 2015. Doctoral Dissertation, University of Melbourne. Accessed March 05, 2021. http://hdl.handle.net/11343/58589.

MLA Handbook (7^th Edition):

Hay, Curtis Mackenzie. “Investigating the role of Gpr62 in oligodendrocyte development and central nervous system myelination.” 2015. Web. 05 Mar 2021.

Vancouver:

Hay CM. Investigating the role of Gpr62 in oligodendrocyte development and central nervous system myelination. [Internet] [Doctoral dissertation]. University of Melbourne; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/11343/58589.

Council of Science Editors:

Hay CM. Investigating the role of Gpr62 in oligodendrocyte development and central nervous system myelination. [Doctoral Dissertation]. University of Melbourne; 2015. Available from: http://hdl.handle.net/11343/58589

University of Melbourne

24. Govier-Cole, Alistair Evan. Bone morphogenetic protein-4 signalling in glial cells of the central nervous system.

Degree: 2017, University of Melbourne

URL: http://hdl.handle.net/11343/208773

► Multiple sclerosis (MS) affects over 20,000 Australians and over 2-3 million people globally. MS is a demyelinating disease of the central nervous system (CNS) in… (more)

▼ Multiple sclerosis (MS) affects over 20,000 Australians and over 2-3 million people globally. MS is a demyelinating disease of the central nervous system (CNS) in which the insulating myelin sheath of the neuron is degraded. This leads to severe impairment of neuronal signal transmission throughout the CNS. Oligodendrocytes are specialised cells of the CNS that form the myelin sheath. Oligodendrocyte progenitor cells (OPCs) are present in the adult brain and respond to demyelinating injury, but these cells often fail to differentiate from precursor cells into oligodendrocytes to replace damaged myelin in MS lesions. One group of factors linked to this ‘differentiation block’ is the bone morphogenetic protein (BMP) family. This thesis aims to clarify the role of BMP signaling in two major classes of CNS cells: oligodendrocytes, which are formed by OPCs, and astrocytes, which play a role in regulating oligodendrocyte differentiation during CNS injury. Firstly, to understand the influence exerted by BMP4 on oligodendrocytes during remyelination, BMP4 signalling was disrupted by infusing LDN-193189, a pharmacological inhibitor of BMP4 receptors BMPRIA and BMPRIB, following cuprizone-induced demyelination in mice. This resulted in a significantly higher number of mature oligodendrocytes present in the murine corpus callosum after one week of recovery from cuprizone treatment. Furthermore, this increase in oligodendrocyte number was coupled with a significant increase in the degree of remyelinated myelin sheaths in the murine corpus callosum. In vitro analysis demonstrated that LDN-193189 has a direct positive influence on OPC differentiation into mature oligodendrocytes, and reduces the astrogliogenic effect of BMP4. Inhibiting BMP4 signalling in OPCs in vitro also promoted myelination in a dorsal root ganglion co-culture experiment. Analysis of gene transcription in OPCs treated with BMP4 and LDN-193189 suggested that the positive effect of pharmacologically inhibiting BMP4 on oligodendrocyte differentiation and myelination was mediated by downregulation of a DNA binding protein, ID4. This protein has been previously shown to inhibit oligodendrocyte differentiation in response to BMP4 signalling activity. To further understand the signalling mechanisms by which BMP4 elicits its inhibitory effect on oligodendrocyte differentiation, a transgenic mouse with an inducible conditional deletion of Bmpr1a was used to disrupt BMP4 signalling through BMPRIA. Cultures of OPCs with a BMPRIA deletion recapitulated most of the positive effects observed on oligodendrocyte differentiation and myelination as seen in OPCs treated with LDN-193189. This suggested that BMPRIA may exert a critical influence in transmitting the inhibitory BMP4 signal in OPCs compared to BMPRIB. Secondly, the influence exerted by BMP4 signalling on astrocytes was assessed using in vitro and in vivo techniques. Mature astrocyte cultures responded to BMP4 by increasing their proliferation and transcription of Gfap, a key intermediate filament protein that…

Subjects/Keywords: oligodendrocyte; astrocyte; demyelination; remyelination; central nervous system.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Govier-Cole, A. E. (2017). Bone morphogenetic protein-4 signalling in glial cells of the central nervous system. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/208773

Chicago Manual of Style (16^th Edition):

Govier-Cole, Alistair Evan. “Bone morphogenetic protein-4 signalling in glial cells of the central nervous system.” 2017. Doctoral Dissertation, University of Melbourne. Accessed March 05, 2021. http://hdl.handle.net/11343/208773.

MLA Handbook (7^th Edition):

Govier-Cole, Alistair Evan. “Bone morphogenetic protein-4 signalling in glial cells of the central nervous system.” 2017. Web. 05 Mar 2021.

Vancouver:

Govier-Cole AE. Bone morphogenetic protein-4 signalling in glial cells of the central nervous system. [Internet] [Doctoral dissertation]. University of Melbourne; 2017. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/11343/208773.

Council of Science Editors:

Govier-Cole AE. Bone morphogenetic protein-4 signalling in glial cells of the central nervous system. [Doctoral Dissertation]. University of Melbourne; 2017. Available from: http://hdl.handle.net/11343/208773

University of Limerick

25. Uszynski, Marcin Kacper. Whole body vibration to address motor and sensory impairments in people with multiple sclerosis.

Degree: 2014, University of Limerick

URL: http://hdl.handle.net/10344/4240

►

peer-reviewed

Multiple Sclerosis (MS) is a progressive degenerative condition of the central nervous system which affects both motor and sensory components. Common symptoms include muscle… (more)

▼

peer-reviewed

Multiple Sclerosis (MS) is a progressive degenerative condition of the central nervous system which affects both motor and sensory components. Common symptoms include muscle weakness, balance and mobility problems, fatigue, and sensory problems. There is a strong body of evidence that exercise intervention can be beneficial for people with MS (PwMS). However there is very little evidence in the MS literature about treatments that may target the sensory system. Whole Body Vibration (WBV) is a technology that has potential to influence the motor and sensory systems due to its mechanism. Vibration stimulus is delivered through the mechanoreceptors of the feet and stimulates muscle spindle activity what enhances muscle contraction. WBV intervention has been suggested to have a beneficial effect on muscle strength, balance, flexibility and bone mineral density in healthy populations. Initially, a systematic review of the literature was undertaken to examine the effects of WBV intervention in neurological populations. The findings of this review suggested insufficient evidence of the effects of WBV intervention when compared to no intervention or to other treatments. It has also highlighted a number of limitations in the reviewed studies, such as lack of using “gold standard” tools, high variability of study protocols or lack of blind assessors. One of the main concerns in the systematic review was that only one study had looked at changes in sensation after WBV intervention. In order to assess changes in the sensory system post exercise intervention, reliable measurement tools are essential. However, only one study investigated reliability of sensory tools in PwMS. Therefore, test-retest and inter-rater reliability studies of four sensory measures in PwMS were carried out. The findings from these studies indicated that the ICC values for the Neurothesiometer (NT) and Verbal Analogue Scale (VAS) for sensation were high and these two scales should be considered for measuring changes in sensation in ambulatory PwMS. Sensory information plays an important role in motor control and in providing feedback required to perform motor tasks, such as walking or to control balance. The next study investigated the relationship between foot vibration threshold and walking and balance in PwMS. Findings revealed that foot vibration threshold measured with NT has good to moderate relationship with the Berg balance scale, the 6 minute walking test and the Timed Up and Go test. This study has also provided the preliminary evidence that vibration threshold can distinguish between those PwMS with and without walking limitations. Taking into account the findings from literature review, the RCT used a “gold standard” tool to measure strength, a reliable tool to measure changes in vibration threshold and a novel, more comprehensive tool to measure changes in balance. It investigated the feasibility and effectiveness of 12 weeks of WBV intervention on muscle strength, sensation and other clinical measures in PwMS. Findings…

Advisors/Committee Members: Coote, Susan, Donnelly, Alan Edward, IRC.

Subjects/Keywords: MS; multiple scelerosis; central nervous system

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APA (6^th Edition):

Uszynski, M. K. (2014). Whole body vibration to address motor and sensory impairments in people with multiple sclerosis. (Thesis). University of Limerick. Retrieved from http://hdl.handle.net/10344/4240

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Uszynski, Marcin Kacper. “Whole body vibration to address motor and sensory impairments in people with multiple sclerosis.” 2014. Thesis, University of Limerick. Accessed March 05, 2021. http://hdl.handle.net/10344/4240.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Uszynski, Marcin Kacper. “Whole body vibration to address motor and sensory impairments in people with multiple sclerosis.” 2014. Web. 05 Mar 2021.

Vancouver:

Uszynski MK. Whole body vibration to address motor and sensory impairments in people with multiple sclerosis. [Internet] [Thesis]. University of Limerick; 2014. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10344/4240.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Uszynski MK. Whole body vibration to address motor and sensory impairments in people with multiple sclerosis. [Thesis]. University of Limerick; 2014. Available from: http://hdl.handle.net/10344/4240

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

California State University – Sacramento

26. Croteau, Christopher. Inducing ASPA expression in astroglia and the role of SOX2 in glial cell development.

Degree: MA, Biological Science, 2016, California State University – Sacramento

URL: http://hdl.handle.net/10211.3/171323

► Canavan disease (CD) is an autosomal recessive neurodegenerative disorder that begins in infancy and causes death by early childhood. CD is typified by a loss… (more)

▼ Canavan disease (CD) is an autosomal recessive neurodegenerative disorder that begins in infancy and causes death by early childhood. CD is typified by a loss of white matter and astrogliosis in the brain, which are caused by inactivating mutations in the gene that encodes aspartoacylase (ASPA). Normally, ASPA metabolizes N-acetyl-L-aspartic acid (NAA). Research indicates the consequent increase in NAA that occurs in the absence of functional ASPA causes the white matter degeneration and astrogliosis observed in CD. Another neurological phenotype caused by high levels of NAA in CD is dysmyelination of the CNS and increased oligodendrocyte death. Because the molecular etiology of CD phenotypes is increased NAA, the most effective treatment for afflicted infants would likely be to permanently reduce the levels of NAA in the CNS and, thereby, help promote remyelination. One major goal of this research project was to generate ASPA-expressing astroglia from human induced pluripotent stem cells (hiPSCs) to determine if they can be used as a therapeutic tool for reducing elevated NAA levels. To remyelinate the CNS of CD patients, it will also be important to use oligodendrocytes because they are the only myelinating glial cell in the brain. It is therefore critical to understand the mechanisms used by oligodendrocyte precursor cells (OPCs) to differentiate into terminally differentiated oligodendrocytes. The transcription factor SOX2 maintains stem cell populations and promotes neurogenesis; however, the specific function of SOX2 within the oligodendrocyte lineage is not well understood. Therefore, the second major goal of this research was to elucidate the role SOX2 plays in oligodendrocyte development. First, to determine a pure population of hiPSC-derived astroglia, immunocytochemistry (ICC) was used to identify cells expressing the astroglia markers S100B, CD44, and GFAP. These cells were then transduced with a lentiviral vector carrying the ASPA gene under the control of a constitutive promoter and puromycin was used to specifically select ASPA-expressing astroglia. Subsequent analysis using quantitative RT/PCR indicated that ASPA expression in transduced astroglia was not significantly different from non-transduced astroglia. This result suggested that our ASPA-expressing astroglia were likely not expressing ASPA efficiently enough to be a valuable therapy for reducing NAA levels for CD patients. To determine the function of Sox2 in the oligodendrocyte lineage, Cre-loxP-mediated Sox2 gene deletion was used to eliminate Sox2 expression in PDGFR??+ OPCs in postnatal mice. Postnatal spinal cords and brains were then analyzed. Ablating Sox2 in the PDGFR??+ OPCs led to decline in OPCs, pre-myelinating oligodendrocytes, and mature oligodendrocyte. This decline was due to a lack of proliferative OPCs. There was no difference found in the level of cell apoptosis after Sox2 gene ablation. In addition, myelin basic protein (MBP), and 2', 3???-Cyclic-nucleotide 3'-phosphodiesterase (CNPase), proteins critical for… Advisors/Committee Members: Carter, Rosalee C..

Subjects/Keywords: Canavan disease; Central nervous system myelination; Oligodendrocytes

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APA (6^th Edition):

Croteau, C. (2016). Inducing ASPA expression in astroglia and the role of SOX2 in glial cell development. (Masters Thesis). California State University – Sacramento. Retrieved from http://hdl.handle.net/10211.3/171323

Chicago Manual of Style (16^th Edition):

Croteau, Christopher. “Inducing ASPA expression in astroglia and the role of SOX2 in glial cell development.” 2016. Masters Thesis, California State University – Sacramento. Accessed March 05, 2021. http://hdl.handle.net/10211.3/171323.

MLA Handbook (7^th Edition):

Croteau, Christopher. “Inducing ASPA expression in astroglia and the role of SOX2 in glial cell development.” 2016. Web. 05 Mar 2021.

Vancouver:

Croteau C. Inducing ASPA expression in astroglia and the role of SOX2 in glial cell development. [Internet] [Masters thesis]. California State University – Sacramento; 2016. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10211.3/171323.

Council of Science Editors:

Croteau C. Inducing ASPA expression in astroglia and the role of SOX2 in glial cell development. [Masters Thesis]. California State University – Sacramento; 2016. Available from: http://hdl.handle.net/10211.3/171323

Hong Kong University of Science and Technology

27. Wang, Tienan LIFS. Microglia colonization and maintenance in zebrafish.

Degree: 2017, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-104967 ; https://doi.org/10.14711/thesis-991012530268503412 ; http://repository.ust.hk/ir/bitstream/1783.1-104967/1/th_redirect.html

► Microglia, tissue resident macrophages in the CNS, are involved in diverse biological processes such as removing apoptotic neurons, pruning synaptic formation, regulating neuronal activity and… (more)

Subjects/Keywords: Microglia ; Zebra danio ; Central nervous system

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, T. L. (2017). Microglia colonization and maintenance in zebrafish. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-104967 ; https://doi.org/10.14711/thesis-991012530268503412 ; http://repository.ust.hk/ir/bitstream/1783.1-104967/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wang, Tienan LIFS. “Microglia colonization and maintenance in zebrafish.” 2017. Thesis, Hong Kong University of Science and Technology. Accessed March 05, 2021. http://repository.ust.hk/ir/Record/1783.1-104967 ; https://doi.org/10.14711/thesis-991012530268503412 ; http://repository.ust.hk/ir/bitstream/1783.1-104967/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wang, Tienan LIFS. “Microglia colonization and maintenance in zebrafish.” 2017. Web. 05 Mar 2021.

Vancouver:

Wang TL. Microglia colonization and maintenance in zebrafish. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2017. [cited 2021 Mar 05]. Available from: http://repository.ust.hk/ir/Record/1783.1-104967 ; https://doi.org/10.14711/thesis-991012530268503412 ; http://repository.ust.hk/ir/bitstream/1783.1-104967/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wang TL. Microglia colonization and maintenance in zebrafish. [Thesis]. Hong Kong University of Science and Technology; 2017. Available from: http://repository.ust.hk/ir/Record/1783.1-104967 ; https://doi.org/10.14711/thesis-991012530268503412 ; http://repository.ust.hk/ir/bitstream/1783.1-104967/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rutgers University

28. Chueng, Sy-Tsong Dean, 1988-. Multidimensional hybrid nanomaterial approaches for therapeutic and diagnostic applications.

Degree: PhD, Chemistry and Chemical Biology, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/60094/

►

Nanomaterials are highly versatile and allow us to effectively and dynamically control a myriad of biomedical application from stem cell differentiation to diagnostics and translational… (more)

▼

Nanomaterials are highly versatile and allow us to effectively and dynamically control a myriad of biomedical application from stem cell differentiation to diagnostics and translational therapeutics. While the scientific community has made tremendous strides in understanding disease and treatments, the complexities of disease and injuries still undermine the full realization of therapies. To this end, this dissertation will focus on the approaches within the novel nanotechnology toolbox for addressing multiple challenges in the field of regenerative medicine with the ultimate goal to regrow and reform damaged tissues and organs. Specifically, this dissertation addresses the regeneration of neural tissues within the central nervous system as the regeneration of such tissue is extremely challenging in the first two decades of the 21^st century. The first part of the dissertation will focus on the innovative insoluble extracellular approaches for controlling the differentiation of neural stem cells (NSCs) into neurons and supporting cells such as oligodendrocytes. Traditionally, biologists have focused on introducing exogenous materials such as proteins and chemical factors to induce specific stem cell differentiation. The goal of our novel insoluble nanomaterial approaches is to uncover the interaction between cells and their surrounding environments for differentiation. The second part of the thesis will focus on the clinical translational approaches of nanomaterials. Through a novel, non-viral transient gene manipulation method developed by Prof. Lee research laboratory, NanoScript, a nanoparticle-based synthetic transcription factor was tasked to regenerate axon in spinal cord injury. This demonstration is tremendous progress in regenerative medicine as it holds a promise for the regulation of every gene expression in a living biological system. Finally, this dissertation will focus on the development of highly sensitive, selective, real-time, and non-invasive characterizations of stem cell differentiation. The development of such an approach will have a significant impact on cell-based therapy. By overcoming the destructive nature of traditional cellular characterization methods, the clinicians can confirm the mature differentiation of stem cells before transplantation to completely avoid potential tumor formation. As such, more cell-based therapies will find their ways into clinical applications. Altogether, this dissertation covers the widely collaborative nanomaterial-based approaches from guiding the differentiation of stem cell, biosensing, and non-viral nanoparticle for gene expression regulation, to the transplantable nanofiber-nanomaterial hybrid scaffold with the foundation of nanochemistry with well-defined biochemical, chemical, and physical compositions, shapes, and properties.

Advisors/Committee Members: Lee, Ki-Bum (chair), Brennan, John (internal member), Garfunkel, Eric (internal member), Young, Wise (outside member), School of Graduate Studies.

Subjects/Keywords: Nanostructured materials; Central nervous system – Regeneration

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APA (6^th Edition):

Chueng, Sy-Tsong Dean, 1. (2019). Multidimensional hybrid nanomaterial approaches for therapeutic and diagnostic applications. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60094/

Chicago Manual of Style (16^th Edition):

Chueng, Sy-Tsong Dean, 1988-. “Multidimensional hybrid nanomaterial approaches for therapeutic and diagnostic applications.” 2019. Doctoral Dissertation, Rutgers University. Accessed March 05, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60094/.

MLA Handbook (7^th Edition):

Chueng, Sy-Tsong Dean, 1988-. “Multidimensional hybrid nanomaterial approaches for therapeutic and diagnostic applications.” 2019. Web. 05 Mar 2021.

Vancouver:

Chueng, Sy-Tsong Dean 1. Multidimensional hybrid nanomaterial approaches for therapeutic and diagnostic applications. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Mar 05]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60094/.

Council of Science Editors:

Chueng, Sy-Tsong Dean 1. Multidimensional hybrid nanomaterial approaches for therapeutic and diagnostic applications. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60094/

Columbia University

29. Khrimian, Lori N. The Role of Osteocalcin in the Regulation of Brain Development and Functions.

Degree: 2017, Columbia University

URL: https://doi.org/10.7916/D8F76J62

► The central nervous system controls many physiological processes including energy metabolism, immune response, reproduction, and development. In turn, hormones synthesized in and secreted by peripheral… (more)

▼ The central nervous system controls many physiological processes including energy metabolism, immune response, reproduction, and development. In turn, hormones synthesized in and secreted by peripheral organs can be transported across the blood-brain barrier to modulate the development of the brain, the formation of new neurons, neural activity, behavior, and the secretion of brain-derived hormones. The central control of bone mass, mediated by the adipocyte-derived hormone leptin, has raised questions of whether the skeleton may signal back to the brain. In recent years, the Karsenty laboratory has uncovered the endocrine role of the bone-derived hormone osteocalcin. Through the use of a vast array of genetic tools, the Karsenty lab has discovered that osteocalcin is a potent regulator of glucose homeostasis, adaptation to exercise, energy metabolism, and male fertility. The multifunctional role of osteocalcin led us to hypothesize that it may act as a molecular means of communication between the skeleton and the brain. We asked whether osteocalcin could regulate brain development during embryogenesis and behavioral functions in adulthood. In addressing these questions, we observed that bone-derived osteocalcin crosses the blood-brain barrier, accumulates in discrete parts of the brain including the hippocampus, and binds to several neuronal populations to favor the synthesis of monoamine neurotransmitters (serotonin, dopamine, and norepinephrine), and to impede the synthesis of the inhibitory neurotransmitter, GABA. Osteocalcin-/- mice have increased anxiety and depression and impaired learning and memory when compared to WT littermates. We also uncovered that the absence of maternal osteocalcin during embryogenesis hinders brain development and causes defects in spatial learning and memory in the adult offspring. Upon characterizing the necessity of osteocalcin for brain development and cognitive function, we investigated whether bone health is a determinant of cognition, and whether osteocalcin may be sufficient to reverse age-related cognitive decline. In addressing the first question, we found that impairment in either bone formation or bone resorption negatively impacts both anxiety and memory. In addressing the second question, we found that osteocalcin is also necessary for the beneficial effect of young blood on cognitive functions. Finally, we observed reduced anxiety and improved memory in aged mice receiving osteocalcin peripherally. This action appears to require an increase in brain-derived neurotrophic factor levels in the hippocampus. Against the backdrop of our progressively aging population, it is important for future studies to determine whether osteocalcin may act therapeutically in humans to treat age-related cognitive decline. Additionally, to identify potential drug targets, it is important to fully characterize the molecular mechanism by which osteocalcin acts on neurons.

Subjects/Keywords: Brain – Growth; Central nervous system – Growth; Cognition; Cognitive neuroscience; Central nervous system; Genetics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Khrimian, L. N. (2017). The Role of Osteocalcin in the Regulation of Brain Development and Functions. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8F76J62

Chicago Manual of Style (16^th Edition):

Khrimian, Lori N. “The Role of Osteocalcin in the Regulation of Brain Development and Functions.” 2017. Doctoral Dissertation, Columbia University. Accessed March 05, 2021. https://doi.org/10.7916/D8F76J62.

MLA Handbook (7^th Edition):

Khrimian, Lori N. “The Role of Osteocalcin in the Regulation of Brain Development and Functions.” 2017. Web. 05 Mar 2021.

Vancouver:

Khrimian LN. The Role of Osteocalcin in the Regulation of Brain Development and Functions. [Internet] [Doctoral dissertation]. Columbia University; 2017. [cited 2021 Mar 05]. Available from: https://doi.org/10.7916/D8F76J62.

Council of Science Editors:

Khrimian LN. The Role of Osteocalcin in the Regulation of Brain Development and Functions. [Doctoral Dissertation]. Columbia University; 2017. Available from: https://doi.org/10.7916/D8F76J62

Loughborough University

30. Cordery, Philip. The role of central catecholamines in performance during prolonged exercise in warm conditions.

Degree: PhD, 2013, Loughborough University

URL: http://hdl.handle.net/2134/13638

► Performance during prolonged exercise capacity diminishes with increasing temperatures. The onset of fatigue under these conditions is not adequately explained by peripheral mechanisms. Recently, drugs… (more)

Subjects/Keywords: 612; Central nervous system; Heat strain; Central fatigue; Dopamine; Noradrenaline; Serotonin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cordery, P. (2013). The role of central catecholamines in performance during prolonged exercise in warm conditions. (Doctoral Dissertation). Loughborough University. Retrieved from http://hdl.handle.net/2134/13638

Chicago Manual of Style (16^th Edition):

Cordery, Philip. “The role of central catecholamines in performance during prolonged exercise in warm conditions.” 2013. Doctoral Dissertation, Loughborough University. Accessed March 05, 2021. http://hdl.handle.net/2134/13638.

MLA Handbook (7^th Edition):

Cordery, Philip. “The role of central catecholamines in performance during prolonged exercise in warm conditions.” 2013. Web. 05 Mar 2021.

Vancouver:

Cordery P. The role of central catecholamines in performance during prolonged exercise in warm conditions. [Internet] [Doctoral dissertation]. Loughborough University; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2134/13638.

Council of Science Editors:

Cordery P. The role of central catecholamines in performance during prolonged exercise in warm conditions. [Doctoral Dissertation]. Loughborough University; 2013. Available from: http://hdl.handle.net/2134/13638

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Open Access Theses and Dissertations