subject:(Neuron)

University of Sydney

1. Zhang, Donghao. Automatic Neuron Reconstruction Based on 3D Microscopic Images .

Degree: 2016, University of Sydney

► The digital reconstruction of single neurons from 3D microscopic images plays an important role for understanding the neuron morphology and function. However the accurate automatic… (more)

Subjects/Keywords: 3D Neuron Reconstruction; Neuron Morphology

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APA (6^th Edition):

Zhang, D. (2016). Automatic Neuron Reconstruction Based on 3D Microscopic Images . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/15390

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):

Zhang, Donghao. “Automatic Neuron Reconstruction Based on 3D Microscopic Images .” 2016. Thesis, University of Sydney. Accessed March 04, 2021. http://hdl.handle.net/2123/15390.

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

MLA Handbook (7^th Edition):

Zhang, Donghao. “Automatic Neuron Reconstruction Based on 3D Microscopic Images .” 2016. Web. 04 Mar 2021.

Vancouver:

Zhang D. Automatic Neuron Reconstruction Based on 3D Microscopic Images . [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2123/15390.

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

Council of Science Editors:

Zhang D. Automatic Neuron Reconstruction Based on 3D Microscopic Images . [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/15390

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

Texas A&M University

2. Kantarci, Husniye. Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons.

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

URL: http://hdl.handle.net/1969.1/165917

► Stato-Acoustic Ganglion (SAG) neurons originate from the floor of the otic vesicle during a brief developmental window. They subsequently leave the otic vesicle and undergo… (more)

▼ Stato-Acoustic Ganglion (SAG) neurons originate from the floor of the otic vesicle during a brief developmental window. They subsequently leave the otic vesicle and undergo a phase of migration and proliferation (transit-amplification). Neuroblasts finally differentiate into mature SAG neurons and extend processes to connect sensory cells of the inner ear to the information processing centers in the brain. The goal of this dissertation has been to elucidate mechanisms controlling these diverse events, which have heretofore been only poorly understood. First we showed that a threshold level of Fgf signaling initially sets the neurogenic domain in the otic epithelium. However, the level of Fgf signaling increases during development and becomes inhibitory to otic neurogenesis. Specfically, fgf5 is expressed by accumulating SAG neurons, which serves to terminate specification of new neuroblasts and delay differentiation of transit-amplifying cells. Second, we tested the role of transcription factor tfap2a, which we found is expressed in the neurogenic domain in both zebrafish and chick. Gain and loss-of-function studies revealed that Tfap2a activates expression of bmp7a, which in turn partially inhibits Fgf and Notch signaling. By modulating the inhibitory functions of Fgf and Notch, Tfap2a regulates the duration, amount and speed of SAG development. Third, we investigated the mechanism by which SAG neuroblasts leave the otic epithelium. We showed that Goosecoid (Gsc) regulates epithelial-mesenchymal transition of the otic neuroblasts. Fgf signaling regulates expression of gsc in a region iii partially overlapping with the neurogenic otic domain. The medial marker Pax2a acts in opposition to Gsc and stabilizes otic epithelia in non-neurogenic parts of the otic vesicle. Lastly, we conducted a mutagenesis screen in zebrafish to identify ENU-induced mutations that affect SAG development. We recovered a SAG deficient mutation, termed sagd1 that strongly reduces a subset of SAG neurons required for vestibular (balance) functions. Whole genome sequencing revealed that sagd1 affects the glycolytic enzyme, Phosphoglycerate kinase-1 (Pgk1). Further analysis revealed that Pgk1 acts nonautonomously to augment Fgf signaling during early stages of otic neurogenesis. Together, these studies have uncovered a number of previously unknown mechanisms for dynamic regulation of Fgf to control specification, delamination, and maturation of SAG neurons. Advisors/Committee Members: Riley, Bruce B (advisor), Garcia, Luis Rene (committee member), Lekven, Arne (committee member), Panin, Vladislav (committee member).

Subjects/Keywords: SAG; Neuron

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APA (6^th Edition):

Kantarci, H. (2017). Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/165917

Chicago Manual of Style (16^th Edition):

Kantarci, Husniye. “Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons.” 2017. Doctoral Dissertation, Texas A&M University. Accessed March 04, 2021. http://hdl.handle.net/1969.1/165917.

MLA Handbook (7^th Edition):

Kantarci, Husniye. “Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons.” 2017. Web. 04 Mar 2021.

Vancouver:

Kantarci H. Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1969.1/165917.

Council of Science Editors:

Kantarci H. Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/165917

University of Otago

3. Peacock, Hollie Emma. Fezf2 regulates mature neuron maintenance in vitro .

Degree: 2011, University of Otago

URL: http://hdl.handle.net/10523/2022

► Forebrain embryonic zinc-finger family member 2 (FEZF2) is a transcription factor that is expressed at high levels in corticospinal motor neurons and related subcerebral projection… (more)

▼ Forebrain embryonic zinc-finger family member 2 (FEZF2) is a transcription factor that is expressed at high levels in corticospinal motor neurons and related subcerebral projection neurons from early in development through adulthood. Fezf2 is essential for the development of layer V corticospinal motor neurons, with loss of Fezf2 resulting in a complete absence of corticospinal motor neurons and the corticospinal tract. Despite the continued expression of Fezf2 in the adult brain, a role for Fezf2 in mature neurons has remained elusive. This study primarily aimed to help define the function of Fezf2 in mature projection neuron maintenance in vitro, and identify potential mechanisms of Fezf2 function. To identify FEZF2-related genes, which may contribute to the role of Fezf2 in mature neuron maintenance, microarray analysis was used to identify genes differentially expressed after FEZF2 knockdown in a neural precursor cell line. This analysis revealed potential roles for FEZF2 in neuron projection maintenance and cell survival. Primary neural cultures from transgenic mice expressing GFP under the regulation of the Fezf2 promoter (pFezf2-GFP mice; postnatal day 2) were transduced with one of two Fezf2-shRNAs or non-silencing control viruses co-expressing red fluorescent protein. pFezf2-GFP-positive neurons were analysed by time-lapse imaging or Sholl analysis to quantify projection complexity and length. Fezf2 shRNA expression resulted in at least 53% knockdown of target mRNA, and a significant reduction in projection complexity; both the number of projections and the distance that projections reach from the cell soma. Using time-lapse imaging we found that the majority of cells demonstrating projection retraction died within 96 hours. These results demonstrate that Fezf2 is required for the maintenance of a subset of Fezf2-positive mature cortical projection neurons in vitro. Fezf2 may fulfil this function through potential roles in projection maintenance and/or cell survival. Future experiments to clarify the mechanism of Fezf2 function and test this function in vivo will provide significant new information on the maintenance of cortical neurons in health and disease. Advisors/Committee Members: Hughes, Stephanie (advisor).

Subjects/Keywords: neuron; fezf2

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APA (6^th Edition):

Peacock, H. E. (2011). Fezf2 regulates mature neuron maintenance in vitro . (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/2022

Chicago Manual of Style (16^th Edition):

Peacock, Hollie Emma. “Fezf2 regulates mature neuron maintenance in vitro .” 2011. Masters Thesis, University of Otago. Accessed March 04, 2021. http://hdl.handle.net/10523/2022.

MLA Handbook (7^th Edition):

Peacock, Hollie Emma. “Fezf2 regulates mature neuron maintenance in vitro .” 2011. Web. 04 Mar 2021.

Vancouver:

Peacock HE. Fezf2 regulates mature neuron maintenance in vitro . [Internet] [Masters thesis]. University of Otago; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10523/2022.

Council of Science Editors:

Peacock HE. Fezf2 regulates mature neuron maintenance in vitro . [Masters Thesis]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/2022

University of Debrecen

4. Vincze, Balázs. Béka premotor interneuronok kvantitatív analízise .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2010, University of Debrecen

URL: http://hdl.handle.net/2437/95687

Béka agytörzsi premotor interneuronokat rekonstruáltunk három dimenzióban Neurolucida számítógépes program segítségével Advisors/Committee Members: Birinyi, András (advisor).

Subjects/Keywords: neuron; szóma

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APA (6^th Edition):

Vincze, B. (2010). Béka premotor interneuronok kvantitatív analízise . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/95687

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):

Vincze, Balázs. “Béka premotor interneuronok kvantitatív analízise .” 2010. Thesis, University of Debrecen. Accessed March 04, 2021. http://hdl.handle.net/2437/95687.

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

MLA Handbook (7^th Edition):

Vincze, Balázs. “Béka premotor interneuronok kvantitatív analízise .” 2010. Web. 04 Mar 2021.

Vancouver:

Vincze B. Béka premotor interneuronok kvantitatív analízise . [Internet] [Thesis]. University of Debrecen; 2010. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2437/95687.

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

Council of Science Editors:

Vincze B. Béka premotor interneuronok kvantitatív analízise . [Thesis]. University of Debrecen; 2010. Available from: http://hdl.handle.net/2437/95687

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

University of Waterloo

5. Lloyd, Drew. A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica.

Degree: 2011, University of Waterloo

URL: http://hdl.handle.net/10012/6265

► Aplysia Californica are marine mollusks with a relatively simple central nervous system that makes them ideal for investigating neurons. The bag-cell neuron is found in… (more)

Subjects/Keywords: aplysia; neuron

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APA (6^th Edition):

Lloyd, D. (2011). A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/6265

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):

Lloyd, Drew. “A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica.” 2011. Thesis, University of Waterloo. Accessed March 04, 2021. http://hdl.handle.net/10012/6265.

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

MLA Handbook (7^th Edition):

Lloyd, Drew. “A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica.” 2011. Web. 04 Mar 2021.

Vancouver:

Lloyd D. A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica. [Internet] [Thesis]. University of Waterloo; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10012/6265.

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

Council of Science Editors:

Lloyd D. A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica. [Thesis]. University of Waterloo; 2011. Available from: http://hdl.handle.net/10012/6265

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

University of Guelph

6. Khalid, Aariez. Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex.

Degree: MS, Department of Biomedical Sciences, 2020, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073

► Chronic exposure to ethanol during development may alter the normal structure and function of neurons within the mammalian brain. This thesis focused on effects of… (more)

Subjects/Keywords: Neuron Morphology

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APA (6^th Edition):

Khalid, A. (2020). Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073

Chicago Manual of Style (16^th Edition):

Khalid, Aariez. “Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex.” 2020. Masters Thesis, University of Guelph. Accessed March 04, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073.

MLA Handbook (7^th Edition):

Khalid, Aariez. “Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex.” 2020. Web. 04 Mar 2021.

Vancouver:

Khalid A. Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex. [Internet] [Masters thesis]. University of Guelph; 2020. [cited 2021 Mar 04]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073.

Council of Science Editors:

Khalid A. Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex. [Masters Thesis]. University of Guelph; 2020. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073

University of Melbourne

7. SHIN, YEA SEUL. Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy.

Degree: 2016, University of Melbourne

URL: http://hdl.handle.net/11343/103644

► Neurones are essential for brain homeostasis and as highly metabolic cells rely on mitochondrial oxidative phosphorylation (OXPHOS) for energy. The integrity and functionality of mitochondria… (more)

▼ Neurones are essential for brain homeostasis and as highly metabolic cells rely on mitochondrial oxidative phosphorylation (OXPHOS) for energy. The integrity and functionality of mitochondria are critical for neuronal survival, and the involvement of dysfunctional mitochondria is recognized as a common theme amongst various neuropathologies. New evidence has suggested that the inappropriate clearance of dysfunctional mitochondria via autophagy (termed mitophagy) determines the pathogenesis of neurodegenerative diseases such as Parkinson’s disease. Mechanistic studies of mitophagy have been undertaken using mammalian cell lines, but this research lacks relevance to neuropathologies. This thesis investigates triggers of autophagy/mitophagy in primary neurones, and specifically if disruption of mitochondrial bioenergetics triggers neuronal autophagy, and mitophagy in particular. Cultures of primary cerebellar granule cells (CGCs) were utilized and inhibitors of the OXPHOS complexes (rotenone, 3-Nitropropionic acid, antimycin A, potassium cyanide and oligomycin targeting complex I-V, respectively), were employed to induce bioenergetic dysfunction of mitochondria. Initial investigations using MTT cell viability assay, phase contrast microscopy and cellular membrane permeabilization detected by propidium iodide staining, determined appropriate concentrations of OXPHOS inhibitors which induced effective mitochondrial damage producing slow neuronal degeneration. From this baseline adverse effects of OXPHOS inhibitors on mitochondrial bioenergetics were documented by monitoring reductions in cellular ATP level, mitochondrial membrane potential (ΔΨm) and oxygen consumption rate (OCR) of CGCs. ΔΨm was rapidly dissipated in CGCs exposed to the inhibitors of complexes I, III and IV (rotenone, antimycin A and potassium cyanide, respectively), whilst the inhibitor of complex II, 3- Nitropropionic acid, produced a much slower reduction of ΔΨm. Employing Seahorse XF24 technology allowed an incisive readout of mitochondrial functional changes where significant bioenergetic impairment was observed subsequent to inhibition of complexes I and II, which are core components of energy metabolism regulating the redox balance (NAD+/NADH levels) and TCA cycle. Existent evidence indicates depolarization of ΔΨm triggers mitophagy in mammalian cell lines, however CGCs display contrasting results where ΔΨm depolarization via complex III and IV inhibition was insufficient to elicit mitophagy despite the inducer of mitophagy, PINK1, being mobilized to mitochondria. In contrast, inhibition of complexes I and II induced mitophagy, as indicated by PINK1 mobilization and disappearance of the pH-sensitive fluorescence mitophagy reporter, mt-Rosella. Western immunoblotting of the general autophagy marker, LC3, and monitoring of acidic vesicles with monodansylcadaverine revealed activation of autophagic flux in CGCs exposed to inhibitors of complexes I-IV, indicating general autophagy in response to bioenergetic impairment irrespective of…

Subjects/Keywords: neuron; mitophagy; autophagy; neurodegeneration; primary neuron; bioenergetic

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APA (6^th Edition):

SHIN, Y. S. (2016). Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/103644

Chicago Manual of Style (16^th Edition):

SHIN, YEA SEUL. “Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy.” 2016. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/103644.

MLA Handbook (7^th Edition):

SHIN, YEA SEUL. “Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy.” 2016. Web. 04 Mar 2021.

Vancouver:

SHIN YS. Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy. [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/103644.

Council of Science Editors:

SHIN YS. Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy. [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/103644

University of Rochester

8. Strait, Caleb E. Neural mechanisms of reward-based choice.

Degree: PhD, 2016, University of Rochester

URL: http://hdl.handle.net/1802/30861

► The ability to choose among potential rewards is a vital function of the mind, although our understanding of the biological mechanisms behind this process is… (more)

Subjects/Keywords: Reward; Neuron; Choice

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APA (6^th Edition):

Strait, C. E. (2016). Neural mechanisms of reward-based choice. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/30861

Chicago Manual of Style (16^th Edition):

Strait, Caleb E. “Neural mechanisms of reward-based choice.” 2016. Doctoral Dissertation, University of Rochester. Accessed March 04, 2021. http://hdl.handle.net/1802/30861.

MLA Handbook (7^th Edition):

Strait, Caleb E. “Neural mechanisms of reward-based choice.” 2016. Web. 04 Mar 2021.

Vancouver:

Strait CE. Neural mechanisms of reward-based choice. [Internet] [Doctoral dissertation]. University of Rochester; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1802/30861.

Council of Science Editors:

Strait CE. Neural mechanisms of reward-based choice. [Doctoral Dissertation]. University of Rochester; 2016. Available from: http://hdl.handle.net/1802/30861

9. Kwon, Deborah YongHyun. Characterization of Survival Motor Neuron (SMN) Protein Degradation.

Degree: PhD, Neuroscience, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320510/

► Spinal muscular atrophy (SMA) is an autosomal recessive neurological disorder characterized by loss of lower motor neurons with resulting skeletal muscle atrophy, and is one… (more)

▼ Spinal muscular atrophy (SMA) is an autosomal recessive neurological disorder characterized by loss of lower motor neurons with resulting skeletal muscle atrophy, and is one of the leading genetic causes of infant death. SMA is a consequence of a deletion or other mutation of the survival of motor neuron-1 (SMN1) gene with preservation of the nearly identical SMN2 gene. The disease is associated with reduced levels of the SMN protein, which has the fundamental role of assembling small nuclear ribonucleoproteins – molecules involved in pre-mRNA splicing (Battle et al, 2006; Lefebvre et al, 1995). In accordance with this function, loss of SMN leads to defects in splicing and affects the range of snRNAs and mRNAs produced in tissues (Gabanella et al, 2007; Zhang et al, 2008). While SMN's role in snRNP biogenesis has been well characterized, it remains uncertain why deletion of this ubiquitously expressed gene causes a progressive loss of motor neurons and a specific neuromuscular phenotype. Studying SMN protein stability may indicate how deficiencies in SMN cause disease. The over-arching aim of this dissertation is to characterize the degradation of the SMN protein. A detailed understanding of this mechanism could provide insight into methods for increasing levels of functional SMN protein as an approach to treatment of SMA. Our studies identified the ubiquitin proteasome system as a major degradative pathway for SMN. Steady-state SMN protein levels were increased in cells treated with proteasome inhibitors, but were unchanged when other degradative pathways were inhibited. This thesis examined the effect of proteasome inhibition on SMN protein levels and the SMA disease phenotype in vivo. Our results in SMA model mice highlighted a critical role for SMN in the central nervous system and showed that SMN increases in peripheral tissues could also improve the disease phenotype. We also identified and characterized a novel E3 ubiquitin ligase for SMN and showed that its targeted knockdown increased SMN in cell culture and ameliorated a neuromuscular defect in a C. elegans SMA model. Our work enhances the understanding of SMN protein degradation and demonstrates how this knowledge may be put to therapeutic use. Advisors/Committee Members: Fischbeck, Kenneth (Director), Chitnis, Ajay (Reader), Fallon, Justin (Reader), Hart, Anne (Reader), Youle, Richard (Reader).

Subjects/Keywords: Survival motor neuron

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APA (6^th Edition):

Kwon, D. Y. (2013). Characterization of Survival Motor Neuron (SMN) Protein Degradation. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320510/

Chicago Manual of Style (16^th Edition):

Kwon, Deborah YongHyun. “Characterization of Survival Motor Neuron (SMN) Protein Degradation.” 2013. Doctoral Dissertation, Brown University. Accessed March 04, 2021. https://repository.library.brown.edu/studio/item/bdr:320510/.

MLA Handbook (7^th Edition):

Kwon, Deborah YongHyun. “Characterization of Survival Motor Neuron (SMN) Protein Degradation.” 2013. Web. 04 Mar 2021.

Vancouver:

Kwon DY. Characterization of Survival Motor Neuron (SMN) Protein Degradation. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2021 Mar 04]. Available from: https://repository.library.brown.edu/studio/item/bdr:320510/.

Council of Science Editors:

Kwon DY. Characterization of Survival Motor Neuron (SMN) Protein Degradation. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320510/

University of Debrecen

10. Sári, Zsanett Mercédesz. Magreceptorok szerepe a neuron differenciációban .

Degree: DE – Általános Orvostudományi Kar, 2014, University of Debrecen

URL: http://hdl.handle.net/2437/194832

► A Retinsav Receptor (RAR) és a Liver-X Receptor (LXR) részt vesz különböző idegsejttípusok kialakulásában, viszont az általuk megvalósuló szabályozás még ismeretlen a neurogenezis korai és… (more)

Subjects/Keywords: magreceptor; neuron differenciáció

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APA (6^th Edition):

Sári, Z. M. (2014). Magreceptorok szerepe a neuron differenciációban . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/194832

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):

Sári, Zsanett Mercédesz. “Magreceptorok szerepe a neuron differenciációban .” 2014. Thesis, University of Debrecen. Accessed March 04, 2021. http://hdl.handle.net/2437/194832.

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

MLA Handbook (7^th Edition):

Sári, Zsanett Mercédesz. “Magreceptorok szerepe a neuron differenciációban .” 2014. Web. 04 Mar 2021.

Vancouver:

Sári ZM. Magreceptorok szerepe a neuron differenciációban . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2437/194832.

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

Council of Science Editors:

Sári ZM. Magreceptorok szerepe a neuron differenciációban . [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/194832

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

University of Florida

11. Kang, Tae Seung. Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.

Degree: PhD, Computer Science - Computer and Information Science and Engineering, 2017, University of Florida

URL: https://ufdc.ufl.edu/UFE0050151

► We consider the problem of feedback control when the controller is constructed solely of deterministic spiking neurons. Although spiking neurons and networks have been the… (more)

Subjects/Keywords: control – neuron – spiking

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APA (6^th Edition):

Kang, T. S. (2017). Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0050151

Chicago Manual of Style (16^th Edition):

Kang, Tae Seung. “Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.” 2017. Doctoral Dissertation, University of Florida. Accessed March 04, 2021. https://ufdc.ufl.edu/UFE0050151.

MLA Handbook (7^th Edition):

Kang, Tae Seung. “Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.” 2017. Web. 04 Mar 2021.

Vancouver:

Kang TS. Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. [Internet] [Doctoral dissertation]. University of Florida; 2017. [cited 2021 Mar 04]. Available from: https://ufdc.ufl.edu/UFE0050151.

Council of Science Editors:

Kang TS. Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. [Doctoral Dissertation]. University of Florida; 2017. Available from: https://ufdc.ufl.edu/UFE0050151

Queens University

12. Steinhart, Lauren. Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons .

Degree: Neuroscience Studies, 2011, Queens University

URL: http://hdl.handle.net/1974/6708

► The superior mesenteric ganglion (SMG) provides sympathetic input to areas of the small intestine, colon, spleen, and mesenteric lymph nodes. Interactions between the nervous and… (more)

▼ The superior mesenteric ganglion (SMG) provides sympathetic input to areas of the small intestine, colon, spleen, and mesenteric lymph nodes. Interactions between the nervous and immune systems in the SMG influence sympathetic regulation of gastrointestinal (GI) and immune function. Previous work in our laboratory has demonstrated changes in SMG neuron activity resulting from exposure to inflammatory mediators such as tumour necrosis factor α (TNFα). The current project focused on interactions between mast cells and sympathetic neurons. Mast cells within the SMG release mediators, including histamine, that can act on neurons and alter their activity. We tested the hypothesis that histamine influences signaling in SMG neurons by inhibiting calcium ion influx during cell depolarization using immunohistochemistry and calcium imaging. Immunohistochemistry revealed H3R on the majority of tyrosine hydroxylase-positive sympathetic neurons in the ganglia. Dissociated neurons were incubated in the ratiometric fluorescent calcium indicator dye Fura-2 acetoxymethyl ester, then superfused with extracellular solution containing histamine receptor agonists (histamine, HTMT, imetit) and antagonists (thioperamide) before being depolarized with a KCL solution (70 mM). Application of both histamine (10 μM) and the H3 receptor agonist imetit (100 nM) caused a decrease in depolarization-induced calcium ion influx. However, the inhibition of calcium ion influx became smaller as the concentration of histamine was increased (100 μM, 1 mM) until the inhibition was no longer statistically significant. Application of H3R antagonist thioperamine (300nM) reversed the inhibition of calcium ion influx caused by histamine (10 μM). Application of H1R & H2R agonist histamine trifluoromethyl toluidide (HTMT) (10 μM) caused an increase in calcium ion influx during depolarization. We conclude that activation of H3R decreases calcium ion influx through voltage-gated calcium ion channels, while activation of H1R / H2R increases calcium ion influx. H3R has a higher affinity for histamine, and therefore is preferentially activated at lower concentrations. Increases in histamine receptor activation may alter SMG input to the spleen, mesenteric lymph nodes, small intestine, and colon, resulting in changes in immune and gut function, such as those described in irritable bowel syndrome.

Subjects/Keywords: Sympathetic Neuron ; Histamine

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APA (6^th Edition):

Steinhart, L. (2011). Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/6708

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):

Steinhart, Lauren. “Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons .” 2011. Thesis, Queens University. Accessed March 04, 2021. http://hdl.handle.net/1974/6708.

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

MLA Handbook (7^th Edition):

Steinhart, Lauren. “Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons .” 2011. Web. 04 Mar 2021.

Vancouver:

Steinhart L. Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons . [Internet] [Thesis]. Queens University; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1974/6708.

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

Council of Science Editors:

Steinhart L. Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons . [Thesis]. Queens University; 2011. Available from: http://hdl.handle.net/1974/6708

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

Colorado State University

13. Popichak, Katriana A. Glial signaling mechanisms in the progression of neuroinflammatory injury.

Degree: PhD, Cell and Molecular Biology, 2018, Colorado State University

URL: http://hdl.handle.net/10217/191273

► The response of glial cells to foreign and endogenous stress signals is extensive. As a result, release of inflammatory factors as means of cellular communication… (more)

▼ The response of glial cells to foreign and endogenous stress signals is extensive. As a result, release of inflammatory factors as means of cellular communication and innate immune function, or neuroinflammation, can contribute to neurodegeneration and increased activation of surrounding glia, often associated with Parkinson's disease (PD). The identification of glial activation as an early event in the progression of neurodegenerative disease that precedes neuronal cell death presents an opportunity for better diagnostic markers, as well as new pathways that could be targeted therapeutically. The transcription factor, Nuclear Factor-kappa B (NF-κB), regulates the expression of multiple neuroinflammatory cytokines and chemokines in activated glial cells but the signaling factors modulating glial-glial and glial-neuronal signaling during neurotoxic injury are poorly understood. Thus, inhibition of NF-κB signaling in glial cells could be a promising therapeutic strategy for the prevention of neuroinflammatory injury. Recently, it was found that selected orphan nuclear receptors in the NR4A family (nerve growth factor-induced-β/NGFI-β), including NR4A1 (Nur77) and NR4A2 (Nurr1), can inhibit the inflammatory effects of NF-κB but there are no approved drugs that target these receptors. In the current studies, we utilized several experimental approaches to target neuroinflammation in cellular models of PD and manganese neurotoxicity in primary glia and in animal models. One of these studies demonstrated that a novel ligand of NR4A1 and NR4A2, 1,1-bis (3'-indolyl) -1-(p-methoxyphenyl) methane (C-DIM5), suppressed NF-κB-dependent inflammatory gene expression in astrocytes following treatment with 1-methyl-4-phenyl-1, 2, 3,6-tetrahydropyridine (MPTP) and the inflammatory cytokines, IFN-γ and TNF-α. These data were further supported by previous studies from our laboratory, which examined efficacy of multiple C-DIM compounds in PD animal and cellular models, including one (C-DIM12) identified as a modulator of Nurr1 activity that also inhibited NF-kB-dependent gene expression in glial cells. Collectively, these data demonstrate that NR4A1/Nur77 and NR4A2/Nurr1 dynamically regulated inflammatory gene expression in glia by modulating the transcriptional activity of NF-κB. An additional study examined the role of NF-κB in manganese (Mn)-induced neurotoxicity by exposing purified microglia, astrocytes (from both wild-type and an astrocyte- specific NF-kB (IKK2) knock-out (KO) mouse) and mixed glial cultures to varying Mn concentrations and then treated neurons with the conditioned media (GCM) of each cell type. In doing so, we showed that mixed glial cultures exposed to Mn enhanced glial activation and neuronal death compared to microglia, wild type astrocytes or IKK2-knockout astrocytes alone or in mixed cultures suggesting that astrocytes are a critical mediator of Mn neurotoxicity through enhanced expression of inflammatory cytokines and chemokines, including those most associated with reactive phenotype such as C3 and CCL2.… Advisors/Committee Members: Tjalkens, Ronald B. (advisor), Bouma, Gerrit J. (committee member), Goodrich, Laurie R. (committee member), Legare, Marie E. (committee member), McLean, Jennifer L. (committee member).

Subjects/Keywords: neuroinflammation; glia; neuron

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APA (6^th Edition):

Popichak, K. A. (2018). Glial signaling mechanisms in the progression of neuroinflammatory injury. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/191273

Chicago Manual of Style (16^th Edition):

Popichak, Katriana A. “Glial signaling mechanisms in the progression of neuroinflammatory injury.” 2018. Doctoral Dissertation, Colorado State University. Accessed March 04, 2021. http://hdl.handle.net/10217/191273.

MLA Handbook (7^th Edition):

Popichak, Katriana A. “Glial signaling mechanisms in the progression of neuroinflammatory injury.” 2018. Web. 04 Mar 2021.

Vancouver:

Popichak KA. Glial signaling mechanisms in the progression of neuroinflammatory injury. [Internet] [Doctoral dissertation]. Colorado State University; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10217/191273.

Council of Science Editors:

Popichak KA. Glial signaling mechanisms in the progression of neuroinflammatory injury. [Doctoral Dissertation]. Colorado State University; 2018. Available from: http://hdl.handle.net/10217/191273

Ruhr Universität Bochum

14. Diykov, Dmitry. Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex.

Degree: 2008, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351

► In der vorliegenden Doktorarbeit konnte zum 1. Mal gezeigt werden, dass in Neuronen des visuellen Cortex albinoter Ratten der Na-K-Cl Kotransporter (NKCC1, Cl- -Aufnahme) im… (more)

Subjects/Keywords: Albinismus; Sehrinde; Aminbuttersäure (gamma-); Neuron

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APA (6^th Edition):

Diykov, D. (2008). Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351

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):

Diykov, Dmitry. “Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex.” 2008. Thesis, Ruhr Universität Bochum. Accessed March 04, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351.

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

MLA Handbook (7^th Edition):

Diykov, Dmitry. “Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex.” 2008. Web. 04 Mar 2021.

Vancouver:

Diykov D. Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex. [Internet] [Thesis]. Ruhr Universität Bochum; 2008. [cited 2021 Mar 04]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351.

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

Council of Science Editors:

Diykov D. Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex. [Thesis]. Ruhr Universität Bochum; 2008. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351

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

Universiteit Utrecht

15. Goossens, R. Mechanisms of selective mRNA transport and translation in neuronal axons.

Degree: 2014, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/291824

► Selectively targeting mRNA to subcellular locations for local translation allows the distal regions of cells to rapidly respond to extracellular cues. In developing neurons, axons… (more)

Subjects/Keywords: Neuron; axon; mRNA; translation; transport

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APA (6^th Edition):

Goossens, R. (2014). Mechanisms of selective mRNA transport and translation in neuronal axons. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/291824

Chicago Manual of Style (16^th Edition):

Goossens, R. “Mechanisms of selective mRNA transport and translation in neuronal axons.” 2014. Masters Thesis, Universiteit Utrecht. Accessed March 04, 2021. http://dspace.library.uu.nl:8080/handle/1874/291824.

MLA Handbook (7^th Edition):

Goossens, R. “Mechanisms of selective mRNA transport and translation in neuronal axons.” 2014. Web. 04 Mar 2021.

Vancouver:

Goossens R. Mechanisms of selective mRNA transport and translation in neuronal axons. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2021 Mar 04]. Available from: http://dspace.library.uu.nl:8080/handle/1874/291824.

Council of Science Editors:

Goossens R. Mechanisms of selective mRNA transport and translation in neuronal axons. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/291824

University of California – Santa Cruz

16. Kmet, Muriel Marie. Differentiation of human embryonic stem cells into Corticofugal projection neurons.

Degree: Molecular Cell and Developmental Biology, 2013, University of California – Santa Cruz

URL: http://www.escholarship.org/uc/item/1jp080qr

► Understanding how neuronal diversity is achieved within the cerebral cortex remains a major challenge in neuroscience. The surge of human embryonic stem cells (hESCs) as… (more)

Subjects/Keywords: Biology; Neurosciences; Fezf2; hESCs; neuron

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APA (6^th Edition):

Kmet, M. M. (2013). Differentiation of human embryonic stem cells into Corticofugal projection neurons. (Thesis). University of California – Santa Cruz. Retrieved from http://www.escholarship.org/uc/item/1jp080qr

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):

Kmet, Muriel Marie. “Differentiation of human embryonic stem cells into Corticofugal projection neurons.” 2013. Thesis, University of California – Santa Cruz. Accessed March 04, 2021. http://www.escholarship.org/uc/item/1jp080qr.

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

MLA Handbook (7^th Edition):

Kmet, Muriel Marie. “Differentiation of human embryonic stem cells into Corticofugal projection neurons.” 2013. Web. 04 Mar 2021.

Vancouver:

Kmet MM. Differentiation of human embryonic stem cells into Corticofugal projection neurons. [Internet] [Thesis]. University of California – Santa Cruz; 2013. [cited 2021 Mar 04]. Available from: http://www.escholarship.org/uc/item/1jp080qr.

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

Council of Science Editors:

Kmet MM. Differentiation of human embryonic stem cells into Corticofugal projection neurons. [Thesis]. University of California – Santa Cruz; 2013. Available from: http://www.escholarship.org/uc/item/1jp080qr

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

University of Tasmania

17. Blizzard, CA. The response of the mature central nervous system to traumatic brain injury .

Degree: 2011, University of Tasmania

URL: https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf

► The mature central nervous system (CNS) is unable to repair following traumatic brain injury (TBI). Intervention is difficult as the pathobiology of the brain following… (more)

▼ The mature central nervous system (CNS) is unable to repair following traumatic brain injury (TBI). Intervention is difficult as the pathobiology of the brain following injury is a complex sequence of events that needs to be fully elucidated. Understanding the endogenous mechanisms evoked by the damaged brain when attempting repair from injury is vital for devising effective therapies to treat brain injury. The current thesis is based upon the hypotheses that ultimately, recovery following trauma will require the induction of neurogenesis and either appropriate regeneration or compensatory plasticity of pre-existing neural pathways and that the mechanisms underlying regeneration of mature axons is fundamentally different to developmental growth. This thesis investigated the reactive and regenerative alterations associated with the neural response to physical injury in the adult mammalian brain. This thesis studies are focused upon the potential for regeneration following injury and how comparable regenerating neurons characteristics are to their developmental counterparts. It investigated the alterations within the damaged neurons and the surrounding brain area which may be indicative of an intrinsic capacity for regeneration including frank neuronal replacement following injury, and the role of the neuronal cytoskeleton in neuronal regenerative events, as the mechanisms underlying these processes are currently poorly understood. This thesis demonstrated that heterogenous populations of cultured cortical neurons are able to survive and regenerate following severe structural injury, suggesting that neurons have an intrinsic capacity for regeneration, regardless of the mode of injury. Additionally, alteration of the intrinsic cytoskeletal environment, through the knockout of the neurofilament light chain protein, decreased the regenerative ability of mature neurons, providing further evidence for the intrinsic regulation of regeneration. Results from this thesis indicate that the growth cones of regenerative sprouts differ from their developmental counterparts in their predominant morphology, their dynamic behaviour and their ability to respond to critical growth factors. These differences between the regenerating and developing growth cones may account for the inability of regenerative sprouting axons to make accurate pathway decisions and successfully respond to trauma. The presence of neurogenesis was investigated following structural injury in vitro, which indicated no evidence of neurogenesis following injury. While focal brain injury in vivo induced proliferation of neural progenitors, immunohistochemistry confirmed that astrocytic but not neuronal, cell proliferation was evoked by focal injury, consistent with the in vitro data. However focal injury induced an axonal regenerative response into the injury site, which was neuronal cell type specific, and significant remodelling in a subpopulation of interneurons away from the injury, demonstrating that the adult cortex is…

Subjects/Keywords: brain; injury; CNS; neuron; regeneration

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APA (6^th Edition):

Blizzard, C. (2011). The response of the mature central nervous system to traumatic brain injury . (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf

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):

Blizzard, CA. “The response of the mature central nervous system to traumatic brain injury .” 2011. Thesis, University of Tasmania. Accessed March 04, 2021. https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf.

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

MLA Handbook (7^th Edition):

Blizzard, CA. “The response of the mature central nervous system to traumatic brain injury .” 2011. Web. 04 Mar 2021.

Vancouver:

Blizzard C. The response of the mature central nervous system to traumatic brain injury . [Internet] [Thesis]. University of Tasmania; 2011. [cited 2021 Mar 04]. Available from: https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf.

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

Council of Science Editors:

Blizzard C. The response of the mature central nervous system to traumatic brain injury . [Thesis]. University of Tasmania; 2011. Available from: https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf

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

Vanderbilt University

18. Clanton, Joshua Aaron. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.

Degree: PhD, Biological Sciences, 2013, Vanderbilt University

URL: http://hdl.handle.net/1803/10639

► Parapineal precursors arise from the medially located pineal complex anlage and migrate to the left side of the brain. Published data implicates Fgf8a in the… (more)

Subjects/Keywords: Left-right asymmetry; neuron; Differentiation

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APA (6^th Edition):

Clanton, J. A. (2013). Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10639

Chicago Manual of Style (16^th Edition):

Clanton, Joshua Aaron. “Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/10639.

MLA Handbook (7^th Edition):

Clanton, Joshua Aaron. “Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.” 2013. Web. 04 Mar 2021.

Vancouver:

Clanton JA. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/10639.

Council of Science Editors:

Clanton JA. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/10639

Penn State University

19. Ma, Ningxin. TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION.

Degree: 2019, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/16624nxm31

► Reprogramming of astrocytes into neurons represents a promising approach to regenerate new neurons for brain repair, but the underlying mechanisms driving this trans-differentiation process are… (more)

▼ Reprogramming of astrocytes into neurons represents a promising approach to regenerate new neurons for brain repair, but the underlying mechanisms driving this trans-differentiation process are not well understood. In previous work, we have demonstrated that astrocytes can be effectively reprogrammed into functional neurons in two ways. The ectopic expression of a single transcription factor NeuroD1 converted reactive astrocytes into neurons both in vitro and in vivo. Moreover, we recently identified four small molecules - CHIR99021, DAPT, LDN193189 and SB431542 - that could reach highly efficient neuronal conversion in cultured human fetal astrocytes. Here we employ the next generation of RNA-sequencing technology to investigate the transcriptome changes during the astrocyte-to-neuron (AtN) conversion process. The four small molecules together can rapidly activate the hedgehog signaling pathway while downregulating many glial genes such as FN1 and MYL9 within 24 hours of treatment. Chemical reprogramming is mediated by several waves of differential gene expression, including upregulation of hedgehog, Wnt/β- catenin, and Notch signaling pathways, together with downregulation of TGF-β and JAK/STAT signaling pathways. Co-expression gene network analyses identify functional gene modules that may directly respond to chemical treatment. In addition, we reveal many well-connected hub genes such as RGMA, neuronatin (NNAT), neurogenin 2 (NEUROG2), NPTX2, MOXD1, JAG1, and GAP43, which may coordinate the chemical reprogramming process. In comparison to chemical administration, use of virus triggers strong inflammation- related gene expression and impedes cell cycle. With a more than 100-fold increase by virus, NeuroD1 also directly upregulate its target genes, including neurotransmitter receptors, MAPK and cAMP signaling pathways. Moreover, network analyses suggest significant NeuroD1-correlated genes such as CABP7 and LRRTM2, and also indicate the extensive interactions between neurogenic genes (e.g. SOX13, NEUROD6) and glial genes (e.g. HHEX, PRDM1). Together, these findings provide critical insights into the molecular cascades triggered by either a combination of small molecules or a proneural transcription factor, and depict a trajectory that gradually reprogram astrocytes into neurons. Understanding the molecular mechanisms of cell fate determination during chemical or transcription factor-mediated reprogramming will be instrumental for further development of an efficient clinical application in the future. Advisors/Committee Members: Gong Chen, Dissertation Advisor/Co-Advisor, Gong Chen, Committee Chair/Co-Chair, Yingwei Mao, Committee Member, Shaun Mahony, Committee Member, Qunhua Li, Outside Member.

Subjects/Keywords: reprogramming; astrocyte; neuron; RNA sequencing

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APA (6^th Edition):

Ma, N. (2019). TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/16624nxm31

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):

Ma, Ningxin. “TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION.” 2019. Thesis, Penn State University. Accessed March 04, 2021. https://submit-etda.libraries.psu.edu/catalog/16624nxm31.

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

MLA Handbook (7^th Edition):

Ma, Ningxin. “TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION.” 2019. Web. 04 Mar 2021.

Vancouver:

Ma N. TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION. [Internet] [Thesis]. Penn State University; 2019. [cited 2021 Mar 04]. Available from: https://submit-etda.libraries.psu.edu/catalog/16624nxm31.

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

Council of Science Editors:

Ma N. TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION. [Thesis]. Penn State University; 2019. Available from: https://submit-etda.libraries.psu.edu/catalog/16624nxm31

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

University of Debrecen

20. Papp, Zsuzsanna. Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2010, University of Debrecen

URL: http://hdl.handle.net/2437/95968

► A nucleus cochlearis (CN) a hallópálya els4 átkapcsolódási helye, melyben az elágazó hallóidegrostok többféle neurontípussal létesítenek szinaptikus kapcsolatot (pl. óriás-, piramis-, Purkinje-szer<- és cartwheel-sejtek). Bár… (more)

▼ A nucleus cochlearis (CN) a hallópálya els4 átkapcsolódási helye, melyben az elágazó hallóidegrostok többféle neurontípussal létesítenek szinaptikus kapcsolatot (pl. óriás-, piramis-, Purkinje-szer<- és cartwheel-sejtek). Bár az egyes sejttípusok általában jól elkülöníthet4k egymástól, bizonyos esetekben komoly nehézségekbe ütközhet az egyértelm< sejtazonosítás. A jelen munka célja a CN két jellegzetes neurontípusának (óriás- és cartwheel-sejtek), és azok nyúlványrendszerének morfometriai jellemzése, és az így nyert paraméterek összehasonlítása volt. A morfometriai analízis végzésére az elektrofiziológiai méréseink során biocitinnel feltöltött sejteket alkalmaztunk, amiket streptavidinnel konjugált Alexa-488 fluorofórral tettünk láthatóvá. Az így „el4hívott” sejtekr4l konfokális mikroszkópos optikai rétegfelvételsorozatot készítettünk (ún. „Z-stack” üzemmód), amikb4l a „NeuronStudio” program segítségével elkészítettük a kérdéses neuronok ún. „térfogati modelljét”. A modell segítségével az egyes sejtek nyúlványrendszerének elágazódását számszer<síthet4 morfológia paraméterekkel tudtuk jellemezni. A sejtek morfológiai leírásánál kiindulási paraméterekként a szóma legnagyobb és legkisebb átmér4jét, a sejttestb4l induló nyúlványok számát, a nyúlványrendszer egészének legnagyobb átmér4jét, és a legnagyobb átmér4re mer4leges maximális átmér4jét határoztuk meg. A sejtek nyúlványrendszerének elágazódottságát részben az egész nyúlványrendszert jellemz4 paraméterekkel, részben az elágazódási rendeket jellemz4 paraméterekkel, továbbá Sholl-analízissel és polárhisztogramm-analízissel igyekeztünk jellemezni. Reményeink szerint a fenti paraméterek konzekvens és pontosan dokumentált meghatározásával mód nyílhat a DCN neuronoknak az eddigieknél pontosabb, a funkcionális sajátságokkal nagyobb mérték< harmóniát mutató morfológiai csoportosítására. Ezt támasztja alá azon megfigyelésünk, ami szerint a fenti paraméterek közül némelyekben jelent4s különbséget mutattunk ki a vizsgált két sejttípus között, ami megkönnyítheti ezen neuronféleségek pontos klasszifikálását. Advisors/Committee Members: Rusznák, Zoltán (advisor).

Subjects/Keywords: neuron; nucleus cochlearis; morfológia

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

APA (6^th Edition):

Papp, Z. (2010). Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/95968

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):

Papp, Zsuzsanna. “Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata .” 2010. Thesis, University of Debrecen. Accessed March 04, 2021. http://hdl.handle.net/2437/95968.

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

MLA Handbook (7^th Edition):

Papp, Zsuzsanna. “Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata .” 2010. Web. 04 Mar 2021.

Vancouver:

Papp Z. Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata . [Internet] [Thesis]. University of Debrecen; 2010. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2437/95968.

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

Council of Science Editors:

Papp Z. Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata . [Thesis]. University of Debrecen; 2010. Available from: http://hdl.handle.net/2437/95968

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

George Mason University

21. Graybeal, Lacey. The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons .

Degree: 2014, George Mason University

URL: http://hdl.handle.net/1920/9097

► Dendrites serve as the primary sites for synaptic and sensory neuronal input and impairments in dendrite morphogenesis can result in various neurological diseases such as… (more)

▼ Dendrites serve as the primary sites for synaptic and sensory neuronal input and impairments in dendrite morphogenesis can result in various neurological diseases such as Rett, Down, and Fragile X Syndromes (Kaufmann & Moser, 2000). Thus, uncovering the cellular and molecular mechanisms that govern dendritogenesis in various neurons is important for advancing our understanding of these diseases. Macroautophagy (hereafter referred to as ‘autophagy’) has emerged as a topic of interest in this area, as postmitotic neurons are known to require high basal autophagy in terms of clearing misfolded and/or damaged organelles. Moreover, defects in basal autophagy have been directly linked to neurodegeneration, including neuronal cell death, axon degeneration, and aberrant synapase development which suggests that autophagy has a neuroprotective function (Shen & Ganetzky, 2009; Wong & Cuervo, 2010; Yang, Coleman, Zhang, Zheng, & Yue, 2013). However, despite a well documented role for autophagy in neuronal survival and axonal development, little is known regarding the role of basal autophagy in mediating dendritic arborization or the mechanisms by which the autophagy pathway may be transcriptionally regulated to mediate differential dendritic homeostasis. Thus, we have investigated these mechanisms by utilizing dendritic arborization (da) neurons in the Drosophila melanogaster peripheral nervous system (PNS), which serve as a powerful model for investigating class specific molecular mechanisms of dendrite development and maintenance (Corty, Matthews, & Grueber, 2009; Jan & Jan, 2010). Preliminary microarray analyses demonstrate that the homeodomain transcription factor Cut positively regulates expression of autophagy related genes (Atg) in da neurons. Due to the native differential expression of Cut across the four da neuron subclasses correlating with distinct levels of dendritic complexity (CI-IV) (Grueber, Jan, & Jan, 2002), the central hypothesis of the studies described herein is that Cut differentially regulates the autophagy pathway as a key mechanism in mediating class specific dendritic homeostasis. By utilizing a combination of in vivo genetics, live confocal microscopy, gene expression analysis, immunohistochemistry, and quantitative neuromorphometry, we investigated the role of basal autophagy in regulating class specific dendrite morphogenesis. Here we establish that basal autophagy is required to promote normal class specific dendrite morphogenesis and that it exerts differential effects across da neuron subclasses. We also demonstrate that key autophagy genes (Atg) are positively regulated, in part, by the transcription factor Cut, and that basal autophagy plays a neuroprotective role in regulating higher order dendritic complexity in neurons expressing Cut, namely CIII and CIV da neurons. Cut-independent effects were also observed in the relatively simple CI neurons, where basal autophagy functions to constrain dendritic arbors. Autophagic dysregulation through loss-of-function (LOF) and gain-of-function (GOF)… Advisors/Committee Members: Cox, Daniel N (advisor).

Subjects/Keywords: dendrite; neuron; autophagy; morphogenesis; Drosophila

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

APA (6^th Edition):

Graybeal, L. (2014). The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons . (Thesis). George Mason University. Retrieved from http://hdl.handle.net/1920/9097

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):

Graybeal, Lacey. “The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons .” 2014. Thesis, George Mason University. Accessed March 04, 2021. http://hdl.handle.net/1920/9097.

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

MLA Handbook (7^th Edition):

Graybeal, Lacey. “The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons .” 2014. Web. 04 Mar 2021.

Vancouver:

Graybeal L. The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons . [Internet] [Thesis]. George Mason University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1920/9097.

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

Council of Science Editors:

Graybeal L. The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons . [Thesis]. George Mason University; 2014. Available from: http://hdl.handle.net/1920/9097

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

University of Toronto

22. Jiang, Ke. The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration.

Degree: 2013, University of Toronto

URL: http://hdl.handle.net/1807/70090

►

Inherited photoreceptor degeneration (IPD) is characterized by progressive death of mutant photoreceptors (PRs). To date, mutations in over 186 genes have been associated with IPD.… (more)

▼

Inherited photoreceptor degeneration (IPD) is characterized by progressive death of mutant photoreceptors (PRs). To date, mutations in over 186 genes have been associated with IPD. Unfortunately, little progress has been made towards treatment to prevent PR death. Here I show that expression of the signal transducer and activator of transcription 3 (STAT3) is increased and activated by tyrosine phosphorylation in both PRs and Müller glia of three mouse models of IPD (Tg(RHO P347S), Prph2rds+/- and Pde6brd1/rd1). To determine whether this endogenous activation of Stat3 expression influence PR degeneration, I genetically manipulated Stat3 expression in these two cell types in three IPD models. PR-specific deletion of Stat3 significantly accelerated PR death in Tg(RHO P347S) and Prph2rds+/- retinas. These data revealed, for the first time, that the increased expression of endogenously activated PR-STAT3 is a survival response in mutant PRs. Accordingly, increases in Stat3 expression may form the basis of a PR protective therapy in IPDs. To examine this hypothesis, I transgenically expressed various Stat3 alleles specifically in the PRs of wild type and IPD mice. The expression of a wild type Stat3 allele or a constitutively active Stat3 allele (Stat3C) in the PRs increased their survival in Tg(RHO P347S) mice at PN30 and in Prph2rds+/- mice at 6 months. Phosphorylation of STAT3 at tyrosine 705 was required for the pro-survival effect as the introduction of a Stat3Y705F allele was not protective. Unexpectedly, the deletion of Stat3 from PRs of Pde6brd1/rd1 mice improved PR survival. The basis for this contrasting result is unclear. However, as with the other two IPD models, PR survival was increased with expression of wild type Stat3 or Stat3C alleles in the PRs of Pde6brd1/rd1 mice. When Stat3 was deleted specifically in Müller glial cells in Prph2rds+/- retinas, a small but significant increase in PR survival was observed at 6 months of age, suggesting that the increased expression of Stat3 in Müller glial in IPDs may be pathogenetic. In summary, I have demonstrated that the increased expression and activation of STAT3 is a survival response in mammalian IPDs, a finding with important therapeutic implications for human retinal degenerations.

PhD

Advisors/Committee Members: McInnes, Roderick, Molecular and Medical Genetics.

Subjects/Keywords: Retina; Photoreceptor; Neuron death; 0317

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

APA (6^th Edition):

Jiang, K. (2013). The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/70090

Chicago Manual of Style (16^th Edition):

Jiang, Ke. “The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration.” 2013. Doctoral Dissertation, University of Toronto. Accessed March 04, 2021. http://hdl.handle.net/1807/70090.

MLA Handbook (7^th Edition):

Jiang, Ke. “The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration.” 2013. Web. 04 Mar 2021.

Vancouver:

Jiang K. The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration. [Internet] [Doctoral dissertation]. University of Toronto; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1807/70090.

Council of Science Editors:

Jiang K. The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration. [Doctoral Dissertation]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/70090

University of New Mexico

23. Bird, Clark. The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons.

Degree: Biomedical Sciences Graduate Program, 2012, University of New Mexico

URL: https://digitalrepository.unm.edu/biom_etds/65

► The KH-type splicing regulatory protein (KSRP) promotes the decay of AU-rich element (ARE) containing mRNAs. Although KSRP is expressed in the developing and mature nervous… (more)

Subjects/Keywords: GAP-43; KSRP; Neuron outgrowth

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

APA (6^th Edition):

Bird, C. (2012). The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/65

Chicago Manual of Style (16^th Edition):

Bird, Clark. “The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons.” 2012. Doctoral Dissertation, University of New Mexico. Accessed March 04, 2021. https://digitalrepository.unm.edu/biom_etds/65.

MLA Handbook (7^th Edition):

Bird, Clark. “The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons.” 2012. Web. 04 Mar 2021.

Vancouver:

Bird C. The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons. [Internet] [Doctoral dissertation]. University of New Mexico; 2012. [cited 2021 Mar 04]. Available from: https://digitalrepository.unm.edu/biom_etds/65.

Council of Science Editors:

Bird C. The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons. [Doctoral Dissertation]. University of New Mexico; 2012. Available from: https://digitalrepository.unm.edu/biom_etds/65

University of Iowa

24. Ulrich, Jason Daniel. The regulaton and function of nuclear factor of activated T-cells in neurons.

Degree: PhD, Pharmacology, 2011, University of Iowa

URL: https://ir.uiowa.edu/etd/2782

► Ca2+-dependent transcription is a fundamental process by which neurons translate activation experience into cellular level adaptations. The nuclear factor of activated T-cells (NFAT) family… (more)

▼ Ca2+-dependent transcription is a fundamental process by which neurons translate activation experience into cellular level adaptations. The nuclear factor of activated T-cells (NFAT) family of proteins comprise four Ca2+/CaN-dependent transcription factors that are widely expressed throughout virtually all tissues. Within neurons, NFAT dependent signaling is critical for axonal development, regulation of synapse number and efficacy, and survival. Furthermore, NFAT is implicated in activity dependent regulation of genes involved in synaptic transmission, learning and memory, mood, and pain sensation. NFAT is activated upon elevations in intracellular Ca2+, which results in CaN -dependent dephosphorylation of multiple serine residues within an N-terminal regulatory region. NFAT dephosphorylation permits NFAT translocation to the nucleus, where it can regulate gene expression, frequently co-operatively with other transcription factors, including AP-1 and MEF2. NFAT activation is opposed or terminated by several kinases, including CK1 and GSK3. Despite the importance of NFAT proteins as regulators of Ca2+-dependent transcription, little is known about the regulation and function of specific NFAT isoforms within neurons. In Aim 1 of this thesis I characterized the differential activation of NFATc3 and NFATc4 in DRG neurons. While NFATc3 rapidly translocates the nucleus upon Ca2+-influx through voltage-gated calcium channels, NFATc4 remained remarkably intransient. Modular substitution of NFATc3 regulatory elements increased the rate or retention of NFATc4, whereas converse substitutions of NFATc4 regulatory elements into NFATc3 decreased NFATc3 nuclear translocation. The activation of NFATc4 appears to be inhibited by preferential phosphorylation by kinases, such as GSK3, which counteract CaN-dependent dephosphorylation. In Aim 2 I investigated the role of NFATc3 in hippocampal neurons. While the majority of NFAT reports in neurons have focused on NFATc4, my data suggest that NFATc3 is the predominantly expressed isoform in hippocampal neurons and is critical for depolarization-induced NFAT target gene expression. I further characterized NFATc3 KO mice in a battery of behavioral assays to test whether loss of NFATc3 expression would affect the baseline anxiety/depression state of the animal, or if NFATc3 was critical for learning and memory. Taken together, my data suggest that NFATc3 is important for NFAT-dependent gene expression in central and peripheral neurons and that distinct regulation of NFAT isoforms within neurons may underlie isoform-specific effects on gene expression. Advisors/Committee Members: Usachev, Yuriy M. (supervisor).

Subjects/Keywords: Calcium; Neuron; NFAT; Transcription; Pharmacology

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

APA (6^th Edition):

Ulrich, J. D. (2011). The regulaton and function of nuclear factor of activated T-cells in neurons. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/2782

Chicago Manual of Style (16^th Edition):

Ulrich, Jason Daniel. “The regulaton and function of nuclear factor of activated T-cells in neurons.” 2011. Doctoral Dissertation, University of Iowa. Accessed March 04, 2021. https://ir.uiowa.edu/etd/2782.

MLA Handbook (7^th Edition):

Ulrich, Jason Daniel. “The regulaton and function of nuclear factor of activated T-cells in neurons.” 2011. Web. 04 Mar 2021.

Vancouver:

Ulrich JD. The regulaton and function of nuclear factor of activated T-cells in neurons. [Internet] [Doctoral dissertation]. University of Iowa; 2011. [cited 2021 Mar 04]. Available from: https://ir.uiowa.edu/etd/2782.

Council of Science Editors:

Ulrich JD. The regulaton and function of nuclear factor of activated T-cells in neurons. [Doctoral Dissertation]. University of Iowa; 2011. Available from: https://ir.uiowa.edu/etd/2782

University of Southern California

25. Mora, Rudy J. Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons.

Degree: PhD, Neuroscience, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015

► Here I describe the development of genetically-encoded probes for visualizing the trafficking of neuronal proteins in living cells. The probes are derived from a diverse… (more)

Subjects/Keywords: probe; calcium; traffic; neuron; CaMKII

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

APA (6^th Edition):

Mora, R. J. (2012). Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015

Chicago Manual of Style (16^th Edition):

Mora, Rudy J. “Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons.” 2012. Doctoral Dissertation, University of Southern California. Accessed March 04, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015.

MLA Handbook (7^th Edition):

Mora, Rudy J. “Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons.” 2012. Web. 04 Mar 2021.

Vancouver:

Mora RJ. Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Mar 04]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015.

Council of Science Editors:

Mora RJ. Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015

University of Tennessee – Knoxville

26. Weiss, Ryan John. Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems.

Degree: MS, Electrical Engineering, 2017, University of Tennessee – Knoxville

URL: https://trace.tennessee.edu/utk_gradthes/4986

► Neuromorphic electronics studies the physical realization of neural networks in discrete circuit components. Hardware implementations of neural networks take advantage of highly parallelized computing power… (more)

Subjects/Keywords: Neuromorphic; Neuron; Memristor; Analog

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APA (6^th Edition):

Weiss, R. J. (2017). Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems. (Thesis). University of Tennessee – Knoxville. Retrieved from https://trace.tennessee.edu/utk_gradthes/4986

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):

Weiss, Ryan John. “Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems.” 2017. Thesis, University of Tennessee – Knoxville. Accessed March 04, 2021. https://trace.tennessee.edu/utk_gradthes/4986.

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

MLA Handbook (7^th Edition):

Weiss, Ryan John. “Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems.” 2017. Web. 04 Mar 2021.

Vancouver:

Weiss RJ. Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems. [Internet] [Thesis]. University of Tennessee – Knoxville; 2017. [cited 2021 Mar 04]. Available from: https://trace.tennessee.edu/utk_gradthes/4986.

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

Council of Science Editors:

Weiss RJ. Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems. [Thesis]. University of Tennessee – Knoxville; 2017. Available from: https://trace.tennessee.edu/utk_gradthes/4986

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

Virginia Tech

27. Bilodeau, Gregory Peter. Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells.

Degree: MS, Computer Science and Applications, 2013, Virginia Tech

URL: http://hdl.handle.net/10919/23328

► This paper provides a fully automated method of finding high-quality seed points in 3D space from a stack of images of neuron cells. These seed… (more)

Subjects/Keywords: Neuron tracing; DIADEM; image analysis

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

APA (6^th Edition):

Bilodeau, G. P. (2013). Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/23328

Chicago Manual of Style (16^th Edition):

Bilodeau, Gregory Peter. “Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells.” 2013. Masters Thesis, Virginia Tech. Accessed March 04, 2021. http://hdl.handle.net/10919/23328.

MLA Handbook (7^th Edition):

Bilodeau, Gregory Peter. “Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells.” 2013. Web. 04 Mar 2021.

Vancouver:

Bilodeau GP. Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells. [Internet] [Masters thesis]. Virginia Tech; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10919/23328.

Council of Science Editors:

Bilodeau GP. Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells. [Masters Thesis]. Virginia Tech; 2013. Available from: http://hdl.handle.net/10919/23328

University of New South Wales

28. Curthoys, Nikki Margarita. Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation.

Degree: Medical Sciences, 2011, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true

► The actin cytoskeleton is crucial for many functions including cell motility, cytokinesis, and vesicle formation. Tropomyosins (Tm) are actin associated proteins which regulate the functional… (more)

▼ The actin cytoskeleton is crucial for many functions including cell motility, cytokinesis, and vesicle formation. Tropomyosins (Tm) are actin associated proteins which regulate the functional capacity of actin filaments. At least 40 Tm isoforms are produced from four genes (αTm, βTm, γTm, and δTm), with differential expression and localisation in tissues, cells and subcellular compartments. As some Tms are potential targets for anti-cancer therapies, one aim of this project was to measure how eliminating one subset of isoforms affected expression of other Tms in brain. Using a knockout (KO) mouse model lacking the γTm-gene 9d exon, regional distributions of Tms were investigated by Western blotting in wild type and 9d KO adult mouse Whole Brain, Cerebellum, Amygdala, Hypothalamus, Cerebral Cortex, Hippocampus, and Olfactory Bulb. KO of γTm-gene isoforms Tm5NM1 and Tm5NM2 was shown to induce upregulation of other γTm-gene products. Regional expression patterns of other Tms, including the δTm-gene product Tm4, were established in brain. A previously unidentified product immunoreactive with the Tm4 antibody was observed and characterised as having similar biochemical properties to Tm4; 2D gel electrophoresis indicated Tm4 and this associated product were both post translationally modified. To investigate Tm4 function in neural cells, rat neuroblastoma cells (B35) were stably transfected with a mammalian vector containing the Tm4 gene. These cells were compared with previously developed B35 clones overexpressing the neuronal isoforms: TmBr1, TmBr2, or TmBr3. Using light microscopy it was shown that while overexpression of these isoforms each induced neurite outgrowth, each had highly specific effects on neurite morphology. Analyses of TmBr2 and Tm4 overexpressing B35 cells by fluorescence activated cell sorting indicated these isoforms could significantly affect cell cycle exit. Quantitative proteomics approaches (LC-MS/MS and iTRAQ) identified proteins affected by overexpression of Tm5NM1, TmBr2, TmBr3, or Tm4 isoforms in B35 cells. These data show for the first time that Tms differentially induce changes in the levels of many other proteins, and Tm expression results in isoform specific profiles of other actin binding proteins (ABP). The actin cytoskeleton underpins neurite outgrowth and branching, and these Tms have been identified as regulators of these events and ABP expression. Advisors/Committee Members: Fath, Thomas, Faculty of Medicine, UNSW, Gunning, Peter, Faculty of Medicine, UNSW.

Subjects/Keywords: Tropomyosin; Actin; Neuron; Cytoskeleton; Differentation

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

APA (6^th Edition):

Curthoys, N. M. (2011). Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Curthoys, Nikki Margarita. “Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation.” 2011. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Curthoys, Nikki Margarita. “Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation.” 2011. Web. 04 Mar 2021.

Vancouver:

Curthoys NM. Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true.

Council of Science Editors:

Curthoys NM. Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true

King Abdullah University of Science and Technology

29. Noutsi, Bakiza Kamal. Correlation between membrane fluidity cellular development and stem cell differentiation.

Degree: Biological and Environmental Sciences and Engineering (BESE) Division, 2016, King Abdullah University of Science and Technology

URL: http://hdl.handle.net/10754/621954

► Cell membranes are made up of a complex structure of lipids and proteins that diffuse laterally giving rise to what we call membrane fluidity. During… (more)

Subjects/Keywords: Neuron; development; stem cell; Differentiation

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

APA (6^th Edition):

Noutsi, B. K. (2016). Correlation between membrane fluidity cellular development and stem cell differentiation. (Thesis). King Abdullah University of Science and Technology. Retrieved from http://hdl.handle.net/10754/621954

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):

Noutsi, Bakiza Kamal. “Correlation between membrane fluidity cellular development and stem cell differentiation.” 2016. Thesis, King Abdullah University of Science and Technology. Accessed March 04, 2021. http://hdl.handle.net/10754/621954.

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

MLA Handbook (7^th Edition):

Noutsi, Bakiza Kamal. “Correlation between membrane fluidity cellular development and stem cell differentiation.” 2016. Web. 04 Mar 2021.

Vancouver:

Noutsi BK. Correlation between membrane fluidity cellular development and stem cell differentiation. [Internet] [Thesis]. King Abdullah University of Science and Technology; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10754/621954.

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

Council of Science Editors:

Noutsi BK. Correlation between membrane fluidity cellular development and stem cell differentiation. [Thesis]. King Abdullah University of Science and Technology; 2016. Available from: http://hdl.handle.net/10754/621954

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

Vanderbilt University

30. Madison, Jennifer Lea. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.

Degree: PhD, Pharmacology, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/12672

► Huntington’s disease is a fatal autosomal dominant neurodegenerative disease caused by an expansion of CAG repeats in the DNA of the Huntingtin gene. The length… (more)

▼ Huntington’s disease is a fatal autosomal dominant neurodegenerative disease caused by an expansion of CAG repeats in the DNA of the Huntingtin gene. The length of the repeat is inversely related to the age of disease onset, however it only accounts for 60% of the variability in the age of onset. Therefore, other genetic and environmental effects contribute to the remaining 40% in the variability in age of onset. Multiple neurodegenerative diseases exhibit alterations in metal ion homeostasis. Research in our laboratories has demonstrated a disease-toxicant interaction between mutant Huntingtin and manganese exposure in vitro. Manganese is an essential trace metal that is necessary for many physiological processes, including neurotransmitter synthesis. In high levels, manganese can be damaging to the brain. Exposure that leads to this damage is typically encountered in an occupational setting such as when welding, smelting or mining manganese. The research described in this dissertation is the first to describe the complex gene-environment interactions between mutant Huntingtin and manganese exposure in vivo. The neurochemical and morphological changes identified herein are complex and exhibit both positive and negative effects. My research also identified the earliest evidence for striatal dendritic pathology in YAC128 mice that occur between 13 and 16 weeks postnatal. Additionally, this is the first research to show gender-specific changes in MSN morphology following manganese exposure. These alterations in neuron morphology were most prevalent when manganese levels were elevated and were not due to differential striatal manganese accumulation. Taken together, these data lay the groundwork for understanding the gene-environment interaction between mutant Huntingtin and Mn exposure. Future studies will further our understanding of this interaction that may one day lead to therapeutic intervention. These studies also reinforce the need to include animals of both genders in experimentation to further our understanding of disease across both genders. Advisors/Committee Members: Malcolm J. Avison (committee member), Gregg D. Stanwood (committee member), Aaron B. Bowman (committee member), Michael Aschner (committee member), Eugenia V. Gurevich (Committee Chair).

Subjects/Keywords: neuron morphology; YAC128; manganese; Huntington's disease; medium spiny neuron; neurochemistry

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

APA (6^th Edition):

Madison, J. L. (2011). Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12672

Chicago Manual of Style (16^th Edition):

Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/12672.

MLA Handbook (7^th Edition):

Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Web. 04 Mar 2021.

Vancouver:

Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/12672.

Council of Science Editors:

Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/12672

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Open Access Theses and Dissertations