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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Zhang D. Automatic Neuron Reconstruction Based on 3D Microscopic Images . [Internet] [Thesis]. University of Sydney; 2016. [cited 2020 Feb 21]. 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

University of Otago

2. 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 February 21, 2020. http://hdl.handle.net/10523/2022.

MLA Handbook (7^th Edition):

Peacock, Hollie Emma. “Fezf2 regulates mature neuron maintenance in vitro .” 2011. Web. 21 Feb 2020.

Vancouver:

Peacock HE. Fezf2 regulates mature neuron maintenance in vitro . [Internet] [Masters thesis]. University of Otago; 2011. [cited 2020 Feb 21]. 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

3. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Vincze B. Béka premotor interneuronok kvantitatív analízise . [Internet] [Thesis]. University of Debrecen; 2010. [cited 2020 Feb 21]. 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

4. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Lloyd D. A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica. [Internet] [Thesis]. University of Waterloo; 2011. [cited 2020 Feb 21]. 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

Texas A&M University

5. 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 February 21, 2020. 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. 21 Feb 2020.

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 2020 Feb 21]. 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 Melbourne

6. 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 February 21, 2020. 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. 21 Feb 2020.

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 2020 Feb 21]. 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

7. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Kwon DY. Characterization of Survival Motor Neuron (SMN) Protein Degradation. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2020 Feb 21]. 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 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 February 21, 2020. http://hdl.handle.net/1802/30861.

MLA Handbook (7^th Edition):

Strait, Caleb E. “Neural mechanisms of reward-based choice.” 2016. Web. 21 Feb 2020.

Vancouver:

Strait CE. Neural mechanisms of reward-based choice. [Internet] [Doctoral dissertation]. University of Rochester; 2016. [cited 2020 Feb 21]. 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

University of Florida

9. 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: http://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 http://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 February 21, 2020. http://ufdc.ufl.edu/UFE0050151.

MLA Handbook (7^th Edition):

Kang, Tae Seung. “Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.” 2017. Web. 21 Feb 2020.

Vancouver:

Kang TS. Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. [Internet] [Doctoral dissertation]. University of Florida; 2017. [cited 2020 Feb 21]. Available from: http://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: http://ufdc.ufl.edu/UFE0050151

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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Sári ZM. Magreceptorok szerepe a neuron differenciációban . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2020 Feb 21]. 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

Queens University

11. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Steinhart L. Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons . [Internet] [Thesis]. Queens University; 2011. [cited 2020 Feb 21]. 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

University of Tasmania

12. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Blizzard C. The response of the mature central nervous system to traumatic brain injury . [Internet] [Thesis]. University of Tasmania; 2011. [cited 2020 Feb 21]. 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

University of New Mexico

13. 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 February 21, 2020. 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. 21 Feb 2020.

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 2020 Feb 21]. 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 Rochester

14. Ding, Qian. The Role of BARHL2 in the Neurogenesis of Mouse Retina and Spinal Cord.

Degree: PhD, 2010, University of Rochester

URL: http://hdl.handle.net/1802/9737

► The evolutionary conserved BarH family of homeodomain transcription factors plays essential roles in cell fate specification, cell differentiation, migration and survival by either activation or… (more)

▼ The evolutionary conserved BarH family of homeodomain transcription factors plays essential roles in cell fate specification, cell differentiation, migration and survival by either activation or repression mechanisms. Barhl2, a member of the Barh gene family, is expressed restrictively in the central nervous system. In the retina, Barhl2 is expressed in developing and mature retinal ganglion cells (RGCs), amacrine cells (ACs) and horizontal cells. Here, to investigate the role of Barhl2 in retinal development, Barhl2 deficient mice were generated. Analysis of AC subtypes in Barhl2 deficient retinas suggests that Barhl2 plays a critical role in AC subtype determination. A significant reduction of glycinergic and GABAergic ACs with a substantial increase in the number of cholinergic ACs was observed in Barhl2-null retinas. Barhl2 is also critical for the development of a normal complement of RGCs. Barhl2 deficiency resulted in the approximate 35% apoptotic RGCs during development. Genetic analysis revealed that Barhl2 functions downstream of the Atoh7-Pou4f2 regulatory pathway and regulates the maturation and/or survival of RGCs. Thus, BARHL2 appears to have numerous roles in retinal development, including regulating neuronal subtype specification, differentiation, and survival. In the spinal cord part, we present evidence showing that BARHL2 is required for the development of dI1 interneurons. Targeted deletion of Barhl2 resulted in a significant reduction in a subset of dI1 interneurons, dI1i, that project the axons ipsilaterally. Utilizing genetic axonal tracing and retrograde tracing method, we found that Barhl2-null dI1i interneurons adopted a dI1c-like contralateral axonal projection and ectopically expressed Lhx2, indicating the dI1i interneurons were transfated to a dI1c identity. Moreover, BARHL2 binds to conserved motifs in Lhx2, suggesting that BARHL2 directly regulates the expression of Lhx2. These results demonstrate the requirement for BARHL2 in the acquisition of dI1 subtype identities and also reveal a genetic hierarchy between progenitors and post-mitotic neurons that drives dI1 interneuron differentiation. This study provides insights into the problem of how the identities of distinct classes of neurons at different positions are controlled within the nervous systems. Our results contribute to a better understanding of transcriptional programs that define neuronal subtype identities and molecular mechanisms that guide distinctive aspects of their subtype-specific properties.

Subjects/Keywords: Transcription Factor; Subtype; Neuron

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APA (6^th Edition):

Ding, Q. (2010). The Role of BARHL2 in the Neurogenesis of Mouse Retina and Spinal Cord. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/9737

Chicago Manual of Style (16^th Edition):

Ding, Qian. “The Role of BARHL2 in the Neurogenesis of Mouse Retina and Spinal Cord.” 2010. Doctoral Dissertation, University of Rochester. Accessed February 21, 2020. http://hdl.handle.net/1802/9737.

MLA Handbook (7^th Edition):

Ding, Qian. “The Role of BARHL2 in the Neurogenesis of Mouse Retina and Spinal Cord.” 2010. Web. 21 Feb 2020.

Vancouver:

Ding Q. The Role of BARHL2 in the Neurogenesis of Mouse Retina and Spinal Cord. [Internet] [Doctoral dissertation]. University of Rochester; 2010. [cited 2020 Feb 21]. Available from: http://hdl.handle.net/1802/9737.

Council of Science Editors:

Ding Q. The Role of BARHL2 in the Neurogenesis of Mouse Retina and Spinal Cord. [Doctoral Dissertation]. University of Rochester; 2010. Available from: http://hdl.handle.net/1802/9737

University of Cincinnati

15. Hsieh, Heidi. Zinc Toxicity in Odora Cells.

Degree: MS, Medicine: Toxicology (Environmental Health), 2011, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1313756131

► Zinc has been touted as a panacea for the common cold. However, there has been some controversy over whether Zicam, an intranasal zinc gluconate gel… (more)

Subjects/Keywords: Toxicology; zinc; olfactory neuron; odora

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APA (6^th Edition):

Hsieh, H. (2011). Zinc Toxicity in Odora Cells. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1313756131

Chicago Manual of Style (16^th Edition):

Hsieh, Heidi. “Zinc Toxicity in Odora Cells.” 2011. Masters Thesis, University of Cincinnati. Accessed February 21, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1313756131.

MLA Handbook (7^th Edition):

Hsieh, Heidi. “Zinc Toxicity in Odora Cells.” 2011. Web. 21 Feb 2020.

Vancouver:

Hsieh H. Zinc Toxicity in Odora Cells. [Internet] [Masters thesis]. University of Cincinnati; 2011. [cited 2020 Feb 21]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1313756131.

Council of Science Editors:

Hsieh H. Zinc Toxicity in Odora Cells. [Masters Thesis]. University of Cincinnati; 2011. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1313756131

Ruhr Universität Bochum

16. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Diykov D. Changes in GABAergic mechanisms and cation-chloride co-transports in the albino visual cortex. [Internet] [Thesis]. Ruhr Universität Bochum; 2008. [cited 2020 Feb 21]. 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

17. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Goossens R. Mechanisms of selective mRNA transport and translation in neuronal axons. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2020 Feb 21]. 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

18. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Kmet MM. Differentiation of human embryonic stem cells into Corticofugal projection neurons. [Internet] [Thesis]. University of California – Santa Cruz; 2013. [cited 2020 Feb 21]. 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 Southern California

19. 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/3010

► 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 (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/3010

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 February 21, 2020. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3010.

MLA Handbook (7^th Edition):

Mora, Rudy J. “Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons.” 2012. Web. 21 Feb 2020.

Vancouver:

Mora RJ. Genetically-encoded probes for visualizing protein trafficking dynamics in living neurons. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2020 Feb 21]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3010.

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/3010

University of Saskatchewan

20. McMillan, Glyn Allan. Sensory coding in an identified motion-sensitive visual neuron of the locust (Locusta migratoria).

Degree: 2009, University of Saskatchewan

URL: http://hdl.handle.net/10388/etd-09302009-142459

► Visual environments may contain a complex combination of object motion. Animals respond to features of complexity by generating adaptive behavioural responses. One important feature of… (more)

▼ Visual environments may contain a complex combination of object motion. Animals respond to features of complexity by generating adaptive behavioural responses. One important feature of a complex visual environment is a rapidly expanding object in the visual field (looming) which may represent an approaching predator or an object on a collision path. Many animals respond to looming objects by generating avoidance behaviours (Maier et al. 2004; Santer et al. 2005; Oliva et al. 2007) and neurons involved in the detection and relay of looming stimuli are present in birds (Sun and Frost 1998) and many insects (Simmons and Rind 1992; Hatsopoulos et al. 1995; Wicklein and Strausfeld 2000). One of the most widely studied visual pathways is found in the locust. This visual pathway, which includes the lobula giant motion detector (LGMD) and its post-synaptic target, the descending contralateral motion detector (DCMD), signals the approach a looming visual stimulus (Schlotterer, 1977; Simmons and Rind, 1992; Hatsopoulos et al., 1995). The DCMD descends through the ventral nerve cord and synapses with motorneurons involved in predator evasion and collision avoidance (Simmons, 1980; Simmons and Rind, 1992; Santer et al., 2006). Previous studies have suggested that this pathway is also affected by more complicated movements in the locust’s visual environment. For example, Guest and Gray (2006) demonstrated that the approach of paired objects in the azimuthal position and approaches at different time intervals affect DCMD firing rate properties. In my first objective of this thesis (Chapter 2), I tested locusts with computer-generated discs that traveled along a combination of non-colliding (translating) and colliding (looming) trajectories and demonstrate how distinctly different DCMD responses result from different trajectory types. In addition to estimating the time of collision and direction of object travel, the presence of a discernable peak associated with the time of object deviation suggests that DCMD responses may contain information related to changes in motion. Previous studies suggest that LGMD/DCMD encodes approaching objects using rate coding; edge expansion of approaching objects causes an increased rate of neuronal firing (Schlotterer, 1977; Hatsopoulos et al., 1995; Judge and Rind, 1997; Gabbiani et al., 1999). Based on observations of DCMD responses to simple looming objects that showed oscillations in DCMD responses (for example, Fig. 1D Santer et al., 2006) and the fact that bursting occurs in many other sensory systems (Yu and Margoliash, 1996; Sherman, 2001; Krahe and Gabbiani, 2004; Marsat and Pollack, 2006), it was hypothesized that the DCMD may show bursting activity. In my second objective of this thesis (Chapter 3), I tested locusts with simple looming stimuli known to generate behavioural responses in order to identify and quantify bursting activity. Results show that the highest frequency of bursts occurred at intervals of 40-50 ms (20-25 Hz). The behavioural significance of this frequency is related… Advisors/Committee Members: Gray, Jack, Fisher, Thomas, Niyogi, Som, Campanucci, Veronica, Chivers, Doug.

Subjects/Keywords: Neuron; DCMD; Vision; Neuroethology; Locust

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APA (6^th Edition):

McMillan, G. A. (2009). Sensory coding in an identified motion-sensitive visual neuron of the locust (Locusta migratoria). (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/etd-09302009-142459

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):

McMillan, Glyn Allan. “Sensory coding in an identified motion-sensitive visual neuron of the locust (Locusta migratoria).” 2009. Thesis, University of Saskatchewan. Accessed February 21, 2020. http://hdl.handle.net/10388/etd-09302009-142459.

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

MLA Handbook (7^th Edition):

McMillan, Glyn Allan. “Sensory coding in an identified motion-sensitive visual neuron of the locust (Locusta migratoria).” 2009. Web. 21 Feb 2020.

Vancouver:

McMillan GA. Sensory coding in an identified motion-sensitive visual neuron of the locust (Locusta migratoria). [Internet] [Thesis]. University of Saskatchewan; 2009. [cited 2020 Feb 21]. Available from: http://hdl.handle.net/10388/etd-09302009-142459.

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

Council of Science Editors:

McMillan GA. Sensory coding in an identified motion-sensitive visual neuron of the locust (Locusta migratoria). [Thesis]. University of Saskatchewan; 2009. Available from: http://hdl.handle.net/10388/etd-09302009-142459

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

Virginia Tech

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

Degree: MS, Computer Science, 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 (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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Bilodeau GP. Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells. [Internet] [Masters thesis]. Virginia Tech; 2013. [cited 2020 Feb 21]. 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 Arizona

22. Schaefer, Jennifer. INTRINSIC PROPERTIES OF LARVAL DROSOPHILA MOTONEURONS AND THEIR CONTRIBUTION TO MOTONEURON RECRUITMENT AND FIRING BEHAVIOR DURING FICTIVE LOCOMOTION .

Degree: 2010, University of Arizona

URL: http://hdl.handle.net/10150/194655

► Locomotion is controlled in large part by neural circuits (CPGs) that generate rhythmic stereotyped outputs in the absence of descending or sensory inputs. The output… (more)

▼ Locomotion is controlled in large part by neural circuits (CPGs) that generate rhythmic stereotyped outputs in the absence of descending or sensory inputs. The output of a neural circuit is determined by the configuration of the circuit, synapse properties, and the intrinsic properties of component neurons. In order to understand how a neural circuit functions component neurons, their connections, and their intrinsic properties must be characterized. Motoneurons are a useful cell in which to begin investigation of CPG function because they are accessible and provide a measure of the cumulative activity of the circuit. Drosophila is a potentially useful model system for the study of motoneuron intrinsic properties, their contribution to locomotion, and of locomotor CPGs because the genetic and molecular techniques available in Drosophila are surpassed in no other organism and because the Drosophila nervous system is small in comparison to vertebrate nervous systems. Further, whole-cell in situ patch clamp recordings from adult and larval motoneurons in relatively intact preparations are possible. Therefore, the first goal of this work was to investigate whether the firing behavior and recruitment of identified Drosophila 1b and 1s motoneurons is analogous to the recruitment of high-threshold, phasic and low-threshold, tonic motoneurons in other organisms. The second goal was to determine whether active conductances influence motoneuron recruitment in response to synaptic input. The final aim was to investigate how these factors influence CPG output to muscles. Findings from current clamp studies indicate that1b motoneurons are more easily recruited than 1s motoneurons, in agreement with the hypothesis that 1b motoneurons are analogous to low-threshold motoneurons described in other organisms. Further, orderly recruitment of Drosophila 1b motoneurons before 1s motoneurons is not a result of passive properties. Instead, the Shal channel that encodes a large portion of IA in motoneuron somatodendritic regions is a critical determinant of delay-to-spike in larval Drosophila motoneurons. These findings are behaviorally-relevant because the same recruitment order is seen in simultaneous recordings from motoneuron pairs recruited by synaptic input. Advisors/Committee Members: Levine, Richard B (advisor), Duch, Carsten (committeemember), Fregosi, Ralph (committeemember), Fuglevand, Andrew (committeemember), Rankin, Lucinda (committeemember).

Subjects/Keywords: Drosophila; excitability; motor neuron; recruitment

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

APA (6^th Edition):

Schaefer, J. (2010). INTRINSIC PROPERTIES OF LARVAL DROSOPHILA MOTONEURONS AND THEIR CONTRIBUTION TO MOTONEURON RECRUITMENT AND FIRING BEHAVIOR DURING FICTIVE LOCOMOTION . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194655

Chicago Manual of Style (16^th Edition):

Schaefer, Jennifer. “INTRINSIC PROPERTIES OF LARVAL DROSOPHILA MOTONEURONS AND THEIR CONTRIBUTION TO MOTONEURON RECRUITMENT AND FIRING BEHAVIOR DURING FICTIVE LOCOMOTION .” 2010. Doctoral Dissertation, University of Arizona. Accessed February 21, 2020. http://hdl.handle.net/10150/194655.

MLA Handbook (7^th Edition):

Schaefer, Jennifer. “INTRINSIC PROPERTIES OF LARVAL DROSOPHILA MOTONEURONS AND THEIR CONTRIBUTION TO MOTONEURON RECRUITMENT AND FIRING BEHAVIOR DURING FICTIVE LOCOMOTION .” 2010. Web. 21 Feb 2020.

Vancouver:

Schaefer J. INTRINSIC PROPERTIES OF LARVAL DROSOPHILA MOTONEURONS AND THEIR CONTRIBUTION TO MOTONEURON RECRUITMENT AND FIRING BEHAVIOR DURING FICTIVE LOCOMOTION . [Internet] [Doctoral dissertation]. University of Arizona; 2010. [cited 2020 Feb 21]. Available from: http://hdl.handle.net/10150/194655.

Council of Science Editors:

Schaefer J. INTRINSIC PROPERTIES OF LARVAL DROSOPHILA MOTONEURONS AND THEIR CONTRIBUTION TO MOTONEURON RECRUITMENT AND FIRING BEHAVIOR DURING FICTIVE LOCOMOTION . [Doctoral Dissertation]. University of Arizona; 2010. Available from: http://hdl.handle.net/10150/194655

University of Debrecen

23. 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 (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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Papp Z. Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata . [Internet] [Thesis]. University of Debrecen; 2010. [cited 2020 Feb 21]. 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

University of Tennessee – Knoxville

24. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Weiss RJ. Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems. [Internet] [Thesis]. University of Tennessee – Knoxville; 2017. [cited 2020 Feb 21]. 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

Vanderbilt University

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

Degree: PhD, Biological Sciences, 2013, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-02282013-210910/ ;

► 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://etd.library.vanderbilt.edu/available/etd-02282013-210910/ ;

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 February 21, 2020. http://etd.library.vanderbilt.edu/available/etd-02282013-210910/ ;.

MLA Handbook (7^th Edition):

Clanton, Joshua Aaron. “Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.” 2013. Web. 21 Feb 2020.

Vancouver:

Clanton JA. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2020 Feb 21]. Available from: http://etd.library.vanderbilt.edu/available/etd-02282013-210910/ ;.

Council of Science Editors:

Clanton JA. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-02282013-210910/ ;

University of New South Wales

26. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Curthoys NM. Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2020 Feb 21]. 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

George Mason University

27. 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 February 21, 2020. 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. 21 Feb 2020.

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 2020 Feb 21]. 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 Iowa

28. 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 February 21, 2020. 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. 21 Feb 2020.

Vancouver:

Ulrich JD. The regulaton and function of nuclear factor of activated T-cells in neurons. [Internet] [Doctoral dissertation]. University of Iowa; 2011. [cited 2020 Feb 21]. 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 Sydney

29. Liu, Siqi. Automating the Reconstruction of Neuron Morphological Models: the Rivulet Algorithm Suite .

Degree: 2017, University of Sydney

URL: http://hdl.handle.net/2123/18167

► The automatic reconstruction of single neuron cells is essential to enable large-scale data-driven investigations in computational neuroscience. The problem remains an open challenge due to… (more)

Subjects/Keywords: Neuron Morphology; 3D Neuron Reconstruction; Computational Neuroscience; Biomedical Image Analysis

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

APA (6^th Edition):

Liu, S. (2017). Automating the Reconstruction of Neuron Morphological Models: the Rivulet Algorithm Suite . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/18167

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):

Liu, Siqi. “Automating the Reconstruction of Neuron Morphological Models: the Rivulet Algorithm Suite .” 2017. Thesis, University of Sydney. Accessed February 21, 2020. http://hdl.handle.net/2123/18167.

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

MLA Handbook (7^th Edition):

Liu, Siqi. “Automating the Reconstruction of Neuron Morphological Models: the Rivulet Algorithm Suite .” 2017. Web. 21 Feb 2020.

Vancouver:

Liu S. Automating the Reconstruction of Neuron Morphological Models: the Rivulet Algorithm Suite . [Internet] [Thesis]. University of Sydney; 2017. [cited 2020 Feb 21]. Available from: http://hdl.handle.net/2123/18167.

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

Council of Science Editors:

Liu S. Automating the Reconstruction of Neuron Morphological Models: the Rivulet Algorithm Suite . [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/18167

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

University of Southern California

30. Mahvash Mohammadi, Mohammad. Emulating variability in the behavior of artificial central neurons.

Degree: PhD, Electrical Engineering, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/204254/rec/2325

► The variability in the behavior of artificial central neurons is the topic of this thesis. Variable behavior has been observed in biological neurons, resulting in… (more)

▼ The variability in the behavior of artificial central neurons is the topic of this thesis. Variable behavior has been observed in biological neurons, resulting in changes in neural behavior that might be useful to capture in neuromorphic circuits. This thesis presents a neuromorphic cortical neuron with two main sources of intrinsic variability; synaptic neurotransmitter release and ion-channel variability, designed to be used in neural networks as part of the BioRC Biomimetic Real-Time Cortex project. This neuron has been designed and simulated using carbon nanotube transistors, one of several nanotechnologies under consideration to meet the challenges of scale presented by the cortex. ❧ Research results suggest that some instances of variability are stochastic, while other studies indicate that some instances of variability are chaotic. In this thesis, both possible sources of variability are considered by embedding either Gaussian noise or a chaotic signal into the neuromorphic or synaptic circuit and observing the results. ❧ Our overarching goal for the BioRC project is to demonstrate complex neural networks that possess memory and learning capability. To this end, we believe the behavior of such networks would be enhanced by the addition of variability. This thesis describes neurotransmitter-release variability and ion-channel variability modeled at the circuit level using carbon nanotube circuit elements. We include two different types of signal variabilities in the circuit, a signal with Gaussian noise and a chaotic signal. For neurotransmitter-release variability these signals are simulated as if they were generated internally in a synapse circuit to vary the neurotransmitter release in an unpredictable manner. Variation in neurotransmitter concentration in the synaptic cleft causes a change in the peak magnitude and duration of the postsynaptic potential. For ion-channel variability, these signals are simulated as if they were generated internally in an axon hillock circuit to change the firing mechanism. The variable signal could force the neuron to fire if the variability strength were sufficient or could prevent the neuron from firing. The variable signal is independent of the post-synaptic potential. When there is no post-synaptic potential applied to the axon hillock (the cell membrane is at resting potential), the variable signal forcing the neuron to fire in fact models spontaneous firing of the neuron. ❧ For Gaussian noise, we include a file in our SPICE simulation consisting of random voltage samples that control neurotransmitter release volume. For chaotic signals, we present a chaotic signal generator circuit design and simulation using carbon nanotube transistor SPICE models, the output of which would likewise control neurotransmitter release. The circuit uses a chaotic piecewise linear one-dimensional map, implemented with switched-current circuits that can operate at high frequencies to generate a chaotic output current. ❧ The results presented in this thesis illustrate that… Advisors/Committee Members: Parker, Alice C. (Committee Chair), Marmarelis, Vasilis Z. (Committee Member), Celikel, Tansu (Committee Member).

Subjects/Keywords: ion-channel variability; synaptic variability; cortical neuron; reliability of spike; chaotic signal; carbon nanotube; noisy neuron; stochastic neuron

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APA (6^th Edition):

Mahvash Mohammadi, M. (2012). Emulating variability in the behavior of artificial central neurons. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/204254/rec/2325

Chicago Manual of Style (16^th Edition):

Mahvash Mohammadi, Mohammad. “Emulating variability in the behavior of artificial central neurons.” 2012. Doctoral Dissertation, University of Southern California. Accessed February 21, 2020. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/204254/rec/2325.

MLA Handbook (7^th Edition):

Mahvash Mohammadi, Mohammad. “Emulating variability in the behavior of artificial central neurons.” 2012. Web. 21 Feb 2020.

Vancouver:

Mahvash Mohammadi M. Emulating variability in the behavior of artificial central neurons. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2020 Feb 21]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/204254/rec/2325.

Council of Science Editors:

Mahvash Mohammadi M. Emulating variability in the behavior of artificial central neurons. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/204254/rec/2325

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