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University of Sydney
1.
Zhang, Donghao.
Automatic Neuron Reconstruction Based on 3D Microscopic Images
.
Degree: 2016, University of Sydney
URL: http://hdl.handle.net/2123/15390
► 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)
▼ 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 neuron reconstruction remains a challenging task due to the varying image quality and the complexity in the arborisation of neurons. In this thesis, a novel automatic neuron reconstruction framework is proposed with image enhancement pipelines, soma volume reconstruction and neuron tree tracing. A Neuron Stalker algorithm is first designed to trace the neuronal tree structure based on local gradient vector flows. A more advanced neuron tracing algorithm, so called Rivulet, is further proposed by performing iterative back-tracking on the results of fast-marching with long branches are iteratively extracted. The proposed automatic neuron reconstruction framework was evaluated with various datasets provided by Diadem challenge and the recent BigNeuron project, and demonstrated great robustness to discontinuous and noisy neuronal structures in 3D microscopic images. It also outperformed the other state-of-the–art methods in terms of accuracy of neuronal morphological reconstruction.
Subjects/Keywords: 3D Neuron Reconstruction;
Neuron Morphology
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MLA ·
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APA (6th 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 (16th Edition):
Zhang, Donghao. “Automatic Neuron Reconstruction Based on 3D Microscopic Images
.” 2016. Thesis, University of Sydney. Accessed March 04, 2021.
http://hdl.handle.net/2123/15390.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Zhang, Donghao. “Automatic Neuron Reconstruction Based on 3D Microscopic Images
.” 2016. Web. 04 Mar 2021.
Vancouver:
Zhang D. Automatic Neuron Reconstruction Based on 3D Microscopic Images
. [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/2123/15390.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Zhang D. Automatic Neuron Reconstruction Based on 3D Microscopic Images
. [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/15390
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University
2.
Kantarci, Husniye.
Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons.
Degree: PhD, Biology, 2017, Texas A&M University
URL: http://hdl.handle.net/1969.1/165917
► Stato-Acoustic Ganglion (SAG) neurons originate from the floor of the otic vesicle during a brief developmental window. They subsequently leave the otic vesicle and undergo…
(more)
▼ Stato-Acoustic Ganglion (SAG) neurons originate from the floor of the otic vesicle during a brief developmental window. They subsequently leave the otic vesicle and undergo a phase of migration and proliferation (transit-amplification). Neuroblasts finally differentiate into mature SAG neurons and extend processes to connect sensory cells of the inner ear to the information processing centers in the brain. The goal of this dissertation has been to elucidate mechanisms controlling these diverse events, which have heretofore been only poorly understood.
First we showed that a threshold level of Fgf signaling initially sets the neurogenic domain in the otic epithelium. However, the level of Fgf signaling increases during development and becomes inhibitory to otic neurogenesis. Specfically, fgf5 is expressed by accumulating SAG neurons, which serves to terminate specification of new neuroblasts and delay differentiation of transit-amplifying cells.
Second, we tested the role of transcription factor tfap2a, which we found is expressed in the neurogenic domain in both zebrafish and chick. Gain and loss-of-function studies revealed that Tfap2a activates expression of bmp7a, which in turn partially inhibits Fgf and Notch signaling. By modulating the inhibitory functions of Fgf and Notch, Tfap2a regulates the duration, amount and speed of SAG development.
Third, we investigated the mechanism by which SAG neuroblasts leave the otic epithelium. We showed that Goosecoid (Gsc) regulates epithelial-mesenchymal transition of the otic neuroblasts. Fgf signaling regulates expression of gsc in a region iii partially overlapping with the neurogenic otic domain. The medial marker Pax2a acts in opposition to Gsc and stabilizes otic epithelia in non-neurogenic parts of the otic vesicle.
Lastly, we conducted a mutagenesis screen in zebrafish to identify ENU-induced mutations that affect SAG development. We recovered a SAG deficient mutation, termed sagd1 that strongly reduces a subset of SAG neurons required for vestibular (balance) functions. Whole genome sequencing revealed that sagd1 affects the glycolytic enzyme, Phosphoglycerate kinase-1 (Pgk1). Further analysis revealed that Pgk1 acts nonautonomously to augment Fgf signaling during early stages of otic neurogenesis.
Together, these studies have uncovered a number of previously unknown mechanisms for dynamic regulation of Fgf to control specification, delamination, and maturation of SAG neurons.
Advisors/Committee Members: Riley, Bruce B (advisor), Garcia, Luis Rene (committee member), Lekven, Arne (committee member), Panin, Vladislav (committee member).
Subjects/Keywords: SAG; Neuron
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Kantarci, Husniye. “Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons.” 2017. Doctoral Dissertation, Texas A&M University. Accessed March 04, 2021.
http://hdl.handle.net/1969.1/165917.
MLA Handbook (7th Edition):
Kantarci, Husniye. “Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons.” 2017. Web. 04 Mar 2021.
Vancouver:
Kantarci H. Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1969.1/165917.
Council of Science Editors:
Kantarci H. Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/165917

University of Otago
3.
Peacock, Hollie Emma.
Fezf2 regulates mature neuron maintenance in vitro
.
Degree: 2011, University of Otago
URL: http://hdl.handle.net/10523/2022
► Forebrain embryonic zinc-finger family member 2 (FEZF2) is a transcription factor that is expressed at high levels in corticospinal motor neurons and related subcerebral projection…
(more)
▼ Forebrain embryonic zinc-finger family member 2 (FEZF2) is a transcription factor that is expressed at high levels in corticospinal motor neurons and related subcerebral projection neurons from early in development through adulthood. Fezf2 is essential for the development of layer V corticospinal motor neurons, with loss of Fezf2 resulting in a complete absence of corticospinal motor neurons and the corticospinal tract. Despite the continued expression of Fezf2 in the adult brain, a role for Fezf2 in mature neurons has remained elusive. This study primarily aimed to help define the function of Fezf2 in mature projection
neuron maintenance in vitro, and identify potential mechanisms of Fezf2 function.
To identify FEZF2-related genes, which may contribute to the role of Fezf2 in mature
neuron maintenance, microarray analysis was used to identify genes differentially expressed after FEZF2 knockdown in a neural precursor cell line. This analysis revealed potential roles for FEZF2 in
neuron projection maintenance and cell survival.
Primary neural cultures from transgenic mice expressing GFP under the regulation of the Fezf2 promoter (pFezf2-GFP mice; postnatal day 2) were transduced with one of two Fezf2-shRNAs or non-silencing control viruses co-expressing red fluorescent protein. pFezf2-GFP-positive neurons were analysed by time-lapse imaging or Sholl analysis to quantify projection complexity and length. Fezf2 shRNA expression resulted in at least 53% knockdown of target mRNA, and a significant reduction in projection complexity; both the number of projections and the distance that projections reach from the cell soma. Using time-lapse imaging we found that the majority of cells demonstrating projection retraction died within 96 hours.
These results demonstrate that Fezf2 is required for the maintenance of a subset of Fezf2-positive mature cortical projection neurons in vitro. Fezf2 may fulfil this function through potential roles in projection maintenance and/or cell survival. Future experiments to clarify the mechanism of Fezf2 function and test this function in vivo will provide significant new information on the maintenance of cortical neurons in health and disease.
Advisors/Committee Members: Hughes, Stephanie (advisor).
Subjects/Keywords: neuron;
fezf2
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Peacock, Hollie Emma. “Fezf2 regulates mature neuron maintenance in vitro
.” 2011. Masters Thesis, University of Otago. Accessed March 04, 2021.
http://hdl.handle.net/10523/2022.
MLA Handbook (7th Edition):
Peacock, Hollie Emma. “Fezf2 regulates mature neuron maintenance in vitro
.” 2011. Web. 04 Mar 2021.
Vancouver:
Peacock HE. Fezf2 regulates mature neuron maintenance in vitro
. [Internet] [Masters thesis]. University of Otago; 2011. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/10523/2022.
Council of Science Editors:
Peacock HE. Fezf2 regulates mature neuron maintenance in vitro
. [Masters Thesis]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/2022

University of Debrecen
4.
Vincze, Balázs.
Béka premotor interneuronok kvantitatív analízise
.
Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2010, University of Debrecen
URL: http://hdl.handle.net/2437/95687
Béka agytörzsi premotor interneuronokat rekonstruáltunk három dimenzióban Neurolucida számítógépes program segítségével
Advisors/Committee Members: Birinyi, András (advisor).
Subjects/Keywords: neuron;
szóma
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❌
APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Vincze, Balázs. “Béka premotor interneuronok kvantitatív analízise
.” 2010. Thesis, University of Debrecen. Accessed March 04, 2021.
http://hdl.handle.net/2437/95687.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Vincze, Balázs. “Béka premotor interneuronok kvantitatív analízise
.” 2010. Web. 04 Mar 2021.
Vancouver:
Vincze B. Béka premotor interneuronok kvantitatív analízise
. [Internet] [Thesis]. University of Debrecen; 2010. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/2437/95687.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Vincze B. Béka premotor interneuronok kvantitatív analízise
. [Thesis]. University of Debrecen; 2010. Available from: http://hdl.handle.net/2437/95687
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Waterloo
5.
Lloyd, Drew.
A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica.
Degree: 2011, University of Waterloo
URL: http://hdl.handle.net/10012/6265
► Aplysia Californica are marine mollusks with a relatively simple central nervous system that makes them ideal for investigating neurons. The bag-cell neuron is found in…
(more)
▼ 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 the Aplysia and is important due to its activity causing the onset of a series of behaviours which culminate in egg laying. The bag-cell neuron is generally not very active but can be stimulated into a long active period known as the afterdischarge in which the neuron releases a hormone that causes egg laying. The afterdischarge is due to a fundamental change in the electrophysiological properties of the bag-cell neuron. The purpose of this thesis is to determine a mathematical model for the electrical activity found in a single bag-cell neuron which can be used to investigate the afterdischarge behaviour.
Subjects/Keywords: aplysia; neuron
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th Edition):
Lloyd, Drew. “A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica.” 2011. Thesis, University of Waterloo. Accessed March 04, 2021.
http://hdl.handle.net/10012/6265.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lloyd, Drew. “A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica.” 2011. Web. 04 Mar 2021.
Vancouver:
Lloyd D. A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica. [Internet] [Thesis]. University of Waterloo; 2011. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/10012/6265.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lloyd D. A Mathematical Model of the Bag-Cell Neuron in Aplysia Californica. [Thesis]. University of Waterloo; 2011. Available from: http://hdl.handle.net/10012/6265
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Guelph
6.
Khalid, Aariez.
Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex.
Degree: MS, Department of Biomedical Sciences, 2020, University of Guelph
URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073
► Chronic exposure to ethanol during development may alter the normal structure and function of neurons within the mammalian brain. This thesis focused on effects of…
(more)
▼ Chronic exposure to ethanol during development may alter the normal structure and function of neurons within the mammalian brain. This thesis focused on effects of developmental ethanol exposure on the structure of pyramidal neurons within the mouse piriform cortex (PC) and the primary somatosensory cortex (S1). Sholl analysis demonstrated that ethanol exposure in the PC reduced dendrite tree size for neurons in female mice at postnatal day (P)15, and also affected dendrite diameter and volume in males at P25. In S1, females and males exhibited no change in dendrite tree size following treatment at P15, however, females exhibited a greater dendrite tree size at P25. Dendrite spine density was altered by ethanol treatment in a sex-dependent manner in the PC and S1. These results suggest that developmental ethanol exposure alters the morphological development of pyramidal neurons within the male and female PC and S1, potentially affecting their normal function.
Advisors/Committee Members: Bailey, Craig (advisor).
Subjects/Keywords: Neuron Morphology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Khalid, A. (2020). Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073
Chicago Manual of Style (16th Edition):
Khalid, Aariez. “Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex.” 2020. Masters Thesis, University of Guelph. Accessed March 04, 2021.
https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073.
MLA Handbook (7th Edition):
Khalid, Aariez. “Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex.” 2020. Web. 04 Mar 2021.
Vancouver:
Khalid A. Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex. [Internet] [Masters thesis]. University of Guelph; 2020. [cited 2021 Mar 04].
Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073.
Council of Science Editors:
Khalid A. Developmental ethanol exposure alters the morphology of pyramidal neurons within regions of the mouse sensory cortex. [Masters Thesis]. University of Guelph; 2020. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/18073

University of Melbourne
7.
SHIN, YEA SEUL.
Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy.
Degree: 2016, University of Melbourne
URL: http://hdl.handle.net/11343/103644
► Neurones are essential for brain homeostasis and as highly metabolic cells rely on mitochondrial oxidative phosphorylation (OXPHOS) for energy. The integrity and functionality of mitochondria…
(more)
▼ Neurones are essential for brain homeostasis and as highly metabolic cells rely on mitochondrial oxidative phosphorylation (OXPHOS) for energy. The integrity and functionality of mitochondria are critical for neuronal survival, and the involvement of dysfunctional mitochondria is recognized as a common theme amongst various neuropathologies. New evidence has suggested that the inappropriate clearance of dysfunctional mitochondria via autophagy (termed mitophagy) determines the pathogenesis of neurodegenerative diseases such as Parkinson’s disease. Mechanistic studies of mitophagy have been undertaken using mammalian cell lines, but this research lacks relevance to neuropathologies. This thesis investigates triggers of autophagy/mitophagy in primary neurones, and specifically if disruption of mitochondrial bioenergetics triggers neuronal autophagy, and mitophagy in particular.
Cultures of primary cerebellar granule cells (CGCs) were utilized and inhibitors of the OXPHOS complexes (rotenone, 3-Nitropropionic acid, antimycin A, potassium cyanide and oligomycin targeting complex I-V, respectively), were employed to induce bioenergetic dysfunction of mitochondria. Initial investigations using MTT cell viability assay, phase contrast microscopy and cellular membrane permeabilization detected by propidium iodide staining, determined appropriate concentrations of OXPHOS inhibitors which induced effective mitochondrial damage producing slow neuronal degeneration. From this baseline adverse effects of OXPHOS inhibitors on mitochondrial bioenergetics were documented by monitoring reductions in cellular ATP level, mitochondrial membrane potential (ΔΨm) and oxygen consumption rate (OCR) of CGCs. ΔΨm was rapidly dissipated in CGCs exposed to the inhibitors of complexes I, III and IV (rotenone, antimycin A and potassium cyanide, respectively), whilst the inhibitor of complex II, 3- Nitropropionic acid, produced a much slower reduction of ΔΨm. Employing Seahorse XF24 technology allowed an incisive readout of mitochondrial functional changes where significant bioenergetic impairment was observed subsequent to inhibition of complexes I and II, which are core components of energy metabolism regulating the redox balance (NAD+/NADH levels) and TCA cycle.
Existent evidence indicates depolarization of ΔΨm triggers mitophagy in mammalian cell lines, however CGCs display contrasting results where ΔΨm depolarization via complex III and IV inhibition was insufficient to elicit mitophagy despite the inducer of mitophagy, PINK1, being mobilized to mitochondria. In contrast, inhibition of complexes I and II induced mitophagy, as indicated by PINK1 mobilization and disappearance of the pH-sensitive fluorescence mitophagy reporter, mt-Rosella. Western immunoblotting of the general autophagy marker, LC3, and monitoring of acidic vesicles with monodansylcadaverine revealed activation of autophagic flux in CGCs exposed to inhibitors of complexes I-IV, indicating general autophagy in response to bioenergetic impairment irrespective of…
Subjects/Keywords: neuron; mitophagy; autophagy; neurodegeneration; primary neuron; bioenergetic
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
SHIN, YEA SEUL. “Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy.” 2016. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021.
http://hdl.handle.net/11343/103644.
MLA Handbook (7th Edition):
SHIN, YEA SEUL. “Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy.” 2016. Web. 04 Mar 2021.
Vancouver:
SHIN YS. Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy. [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/11343/103644.
Council of Science Editors:
SHIN YS. Molecular and cellular insights into mitochondrial contributions to neuronal autophagy: links to energetics and mitophagy. [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/103644

University of Rochester
8.
Strait, Caleb E.
Neural mechanisms of reward-based choice.
Degree: PhD, 2016, University of Rochester
URL: http://hdl.handle.net/1802/30861
► The ability to choose among potential rewards is a vital function of the mind, although our understanding of the biological mechanisms behind this process is…
(more)
▼ 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 still in its
infancy.
Decision neuroscientists have shown that various measures of neural
activity
often covary with estimates of decision value. The brain
might draw upon such a signal
as it makes the physical
calculations underlying choice. This work is an investigation of
single neuron value signal formatting, using both behavioral and
neurophysiological
research. I present evidence for an offer
valuation system in the brain, wherein single
value-sensitive
neurons use a signal format that would allow them to participate in
both
value comparison and reward position tagging. Choice behavior
suggested that neural
codes of value may favor more positively
skewed reward distributions. During economic
choice, neurons in
the ventromedial prefrontal cortex (vmPFC) and ventral striatum
(VS)
signaled offer values with mutual inhibition between value
signals for competing offers,
which would allow for comparison.
Value signals in neurons from these areas, the
orbitofrontal
cortex (OFC), the dorsal anterior cingulate cortex (dACC), and the
subgenual anterior cingulate cortex (sgACC) were also sensitive to
the spatial positions
of both offers and choices, information that
would allow value signals to maintain tags
between rewards and
their spatial positions during comparison.
Subjects/Keywords: Reward; Neuron; Choice
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Strait, Caleb E. “Neural mechanisms of reward-based choice.” 2016. Doctoral Dissertation, University of Rochester. Accessed March 04, 2021.
http://hdl.handle.net/1802/30861.
MLA Handbook (7th Edition):
Strait, Caleb E. “Neural mechanisms of reward-based choice.” 2016. Web. 04 Mar 2021.
Vancouver:
Strait CE. Neural mechanisms of reward-based choice. [Internet] [Doctoral dissertation]. University of Rochester; 2016. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1802/30861.
Council of Science Editors:
Strait CE. Neural mechanisms of reward-based choice. [Doctoral Dissertation]. University of Rochester; 2016. Available from: http://hdl.handle.net/1802/30861
9.
Kwon, Deborah YongHyun.
Characterization of Survival Motor Neuron (SMN) Protein
Degradation.
Degree: PhD, Neuroscience, 2013, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:320510/
► Spinal muscular atrophy (SMA) is an autosomal recessive neurological disorder characterized by loss of lower motor neurons with resulting skeletal muscle atrophy, and is one…
(more)
▼ Spinal muscular atrophy (SMA) is an autosomal
recessive neurological disorder characterized by loss of lower
motor neurons with resulting skeletal muscle atrophy, and is one of
the leading genetic causes of infant death. SMA is a consequence of
a deletion or other mutation of the survival of motor
neuron-1
(SMN1) gene with preservation of the nearly identical SMN2 gene.
The disease is associated with reduced levels of the SMN protein,
which has the fundamental role of assembling small nuclear
ribonucleoproteins – molecules involved in pre-mRNA splicing
(Battle et al, 2006; Lefebvre et al, 1995). In accordance with this
function, loss of SMN leads to defects in splicing and affects the
range of snRNAs and mRNAs produced in tissues (Gabanella et al,
2007; Zhang et al, 2008). While SMN's role in snRNP biogenesis has
been well characterized, it remains uncertain why deletion of this
ubiquitously expressed gene causes a progressive loss of motor
neurons and a specific neuromuscular phenotype. Studying SMN
protein stability may indicate how deficiencies in SMN cause
disease.
The over-arching aim of this dissertation is to characterize
the degradation of the SMN protein. A detailed understanding of
this mechanism could provide insight into methods for increasing
levels of functional SMN protein as an approach to treatment of
SMA. Our studies identified the ubiquitin proteasome system as a
major degradative pathway for SMN. Steady-state SMN protein levels
were increased in cells treated with proteasome inhibitors, but
were unchanged when other degradative pathways were inhibited. This
thesis examined the effect of proteasome inhibition on SMN protein
levels and the SMA disease phenotype in vivo. Our results in SMA
model mice highlighted a critical role for SMN in the central
nervous system and showed that SMN increases in peripheral tissues
could also improve the disease phenotype. We also identified and
characterized a novel E3 ubiquitin ligase for SMN and showed that
its targeted knockdown increased SMN in cell culture and
ameliorated a neuromuscular defect in a C. elegans SMA model. Our
work enhances the understanding of SMN protein degradation and
demonstrates how this knowledge may be put to therapeutic
use.
Advisors/Committee Members: Fischbeck, Kenneth (Director), Chitnis, Ajay (Reader), Fallon, Justin (Reader), Hart, Anne (Reader), Youle, Richard (Reader).
Subjects/Keywords: Survival motor neuron
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Kwon, Deborah YongHyun. “Characterization of Survival Motor Neuron (SMN) Protein
Degradation.” 2013. Doctoral Dissertation, Brown University. Accessed March 04, 2021.
https://repository.library.brown.edu/studio/item/bdr:320510/.
MLA Handbook (7th Edition):
Kwon, Deborah YongHyun. “Characterization of Survival Motor Neuron (SMN) Protein
Degradation.” 2013. Web. 04 Mar 2021.
Vancouver:
Kwon DY. Characterization of Survival Motor Neuron (SMN) Protein
Degradation. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2021 Mar 04].
Available from: https://repository.library.brown.edu/studio/item/bdr:320510/.
Council of Science Editors:
Kwon DY. Characterization of Survival Motor Neuron (SMN) Protein
Degradation. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320510/

University of Debrecen
10.
Sári, Zsanett Mercédesz.
Magreceptorok szerepe a neuron differenciációban
.
Degree: DE – Általános Orvostudományi Kar, 2014, University of Debrecen
URL: http://hdl.handle.net/2437/194832
► A Retinsav Receptor (RAR) és a Liver-X Receptor (LXR) részt vesz különböző idegsejttípusok kialakulásában, viszont az általuk megvalósuló szabályozás még ismeretlen a neurogenezis korai és…
(more)
▼ 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 késői fázisában.Kísérletünkben karakterizáltuk az őssejt-
neuron differenciációt RNS és fehérje szinten, illetve meghatároztuk a differenciáció különböző stádiumaiban az RAR és LXR receptorokkal heterodimert alkotó Retinoid-X Receptor (RXR) kötőhelyeket teljes genom szintjén. Vizsgáltuk továbbá a neurális progenitorokban a ligand-aktivált RAR és LXR által kiváltott génexpressziós változásokat is.
Advisors/Committee Members: Nagy, László (advisor), Debreceni Egyetem (advisor).
Subjects/Keywords: magreceptor;
neuron differenciáció
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MLA ·
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APA (6th 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 (16th Edition):
Sári, Zsanett Mercédesz. “Magreceptorok szerepe a neuron differenciációban
.” 2014. Thesis, University of Debrecen. Accessed March 04, 2021.
http://hdl.handle.net/2437/194832.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sári, Zsanett Mercédesz. “Magreceptorok szerepe a neuron differenciációban
.” 2014. Web. 04 Mar 2021.
Vancouver:
Sári ZM. Magreceptorok szerepe a neuron differenciációban
. [Internet] [Thesis]. University of Debrecen; 2014. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/2437/194832.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sári ZM. Magreceptorok szerepe a neuron differenciációban
. [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/194832
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Florida
11.
Kang, Tae Seung.
Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.
Degree: PhD, Computer Science - Computer and Information Science and Engineering, 2017, University of Florida
URL: https://ufdc.ufl.edu/UFE0050151
► We consider the problem of feedback control when the controller is constructed solely of deterministic spiking neurons. Although spiking neurons and networks have been the…
(more)
▼ 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
subject of several previous studies, analysis has primarily been restricted to a firing rate model. In contrast, we construct a spike timing based deterministic spiking
neuron controller whose control output is one or multiple sparse spike trains. We model the problem formally as a hybrid dynamical system comprised of a closed loop between a plant and a spiking
neuron network controller. The construction differs from classical controllers owing to the fact that the control feedback to the plant is generated by convolving the spike trains with fixed kernels, resulting in a highly constrained and stereotyped control signal. We derive a novel synaptic weight update rule via which the spiking
neuron network controller learns to hold process variables at desired set points. We demonstrate the efficacy of the rule by applying it to the classical control problem of the cart-pole (inverted pendulum) and fish locomotion. Experiments demonstrate that the proposed controller has a larger region of stability as compared to the traditional PID controller, and its trajectories differ qualitatively from those of the PID controller. In addition, the proposed controller with a recurrent network generates sparse spike trains with rates as low as 1.99Hz. ( en )
Advisors/Committee Members: BANERJEE,ARUNAVA (committee chair), ENTEZARI,ALIREZA (committee member), XIA,YE (committee member), PARDALOS,PANAGOTE M (committee member).
Subjects/Keywords: control – neuron – spiking
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kang, T. S. (2017). Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0050151
Chicago Manual of Style (16th Edition):
Kang, Tae Seung. “Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.” 2017. Doctoral Dissertation, University of Florida. Accessed March 04, 2021.
https://ufdc.ufl.edu/UFE0050151.
MLA Handbook (7th Edition):
Kang, Tae Seung. “Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers.” 2017. Web. 04 Mar 2021.
Vancouver:
Kang TS. Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. [Internet] [Doctoral dissertation]. University of Florida; 2017. [cited 2021 Mar 04].
Available from: https://ufdc.ufl.edu/UFE0050151.
Council of Science Editors:
Kang TS. Learning Feedforward and Recurrent Deterministic Spiking Neuron Network Feedback Controllers. [Doctoral Dissertation]. University of Florida; 2017. Available from: https://ufdc.ufl.edu/UFE0050151

Queens University
12.
Steinhart, Lauren.
Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons
.
Degree: Neuroscience Studies, 2011, Queens University
URL: http://hdl.handle.net/1974/6708
► The superior mesenteric ganglion (SMG) provides sympathetic input to areas of the small intestine, colon, spleen, and mesenteric lymph nodes. Interactions between the nervous and…
(more)
▼ The superior mesenteric ganglion (SMG) provides sympathetic input to areas of the small intestine, colon, spleen, and mesenteric lymph nodes. Interactions between the nervous and immune systems in the SMG influence sympathetic regulation of gastrointestinal (GI) and immune function. Previous work in our laboratory has demonstrated changes in SMG neuron activity resulting from exposure to inflammatory mediators such as tumour necrosis factor α
(TNFα). The current project focused on interactions between mast cells and sympathetic neurons.
Mast cells within the SMG release mediators, including histamine, that can act on neurons and alter their activity. We tested the hypothesis that histamine influences signaling in SMG neurons by inhibiting calcium ion influx during cell depolarization using immunohistochemistry and calcium imaging.
Immunohistochemistry revealed H3R on the majority of tyrosine hydroxylase-positive
sympathetic neurons in the ganglia. Dissociated neurons were incubated in the ratiometric fluorescent calcium indicator dye Fura-2 acetoxymethyl ester, then superfused with extracellular solution containing histamine receptor agonists (histamine, HTMT, imetit) and antagonists
(thioperamide) before being depolarized with a KCL solution (70 mM). Application of both
histamine (10 μM) and the H3 receptor agonist imetit (100 nM) caused a decrease in
depolarization-induced calcium ion influx. However, the inhibition of calcium ion influx became smaller as the concentration of histamine was increased (100 μM, 1 mM) until the inhibition was no longer
statistically significant. Application of H3R antagonist thioperamine (300nM) reversed the inhibition of calcium ion influx caused by histamine (10 μM). Application of H1R & H2R agonist histamine trifluoromethyl toluidide (HTMT) (10 μM) caused an increase in calcium ion influx during depolarization. We conclude that activation of H3R decreases calcium ion influx through voltage-gated
calcium ion channels, while activation of H1R / H2R increases calcium ion influx. H3R has a higher affinity for histamine, and therefore is preferentially activated at lower concentrations. Increases in histamine receptor activation may alter SMG input to the spleen, mesenteric lymph nodes, small
intestine, and colon, resulting in changes in immune and gut function, such as those described in irritable bowel syndrome.
Subjects/Keywords: Sympathetic Neuron
;
Histamine
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Steinhart, Lauren. “Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons
.” 2011. Thesis, Queens University. Accessed March 04, 2021.
http://hdl.handle.net/1974/6708.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Steinhart, Lauren. “Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons
.” 2011. Web. 04 Mar 2021.
Vancouver:
Steinhart L. Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons
. [Internet] [Thesis]. Queens University; 2011. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1974/6708.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Steinhart L. Histamine Influences Depolarization-Induced Calcium Ion Influx in Sympathetic Neurons
. [Thesis]. Queens University; 2011. Available from: http://hdl.handle.net/1974/6708
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Colorado State University
13.
Popichak, Katriana A.
Glial signaling mechanisms in the progression of neuroinflammatory injury.
Degree: PhD, Cell and Molecular Biology, 2018, Colorado State University
URL: http://hdl.handle.net/10217/191273
► The response of glial cells to foreign and endogenous stress signals is extensive. As a result, release of inflammatory factors as means of cellular communication…
(more)
▼ The response of glial cells to foreign and endogenous stress signals is extensive. As a result, release of inflammatory factors as means of cellular communication and innate immune function, or neuroinflammation, can contribute to neurodegeneration and increased activation of surrounding glia, often associated with Parkinson's disease (PD). The identification of glial activation as an early event in the progression of neurodegenerative disease that precedes neuronal cell death presents an opportunity for better diagnostic markers, as well as new pathways that could be targeted therapeutically. The transcription factor, Nuclear Factor-kappa B (NF-κB), regulates the expression of multiple neuroinflammatory cytokines and chemokines in activated glial cells but the signaling factors modulating glial-glial and glial-neuronal signaling during neurotoxic injury are poorly understood. Thus, inhibition of NF-κB signaling in glial cells could be a promising therapeutic strategy for the prevention of neuroinflammatory injury. Recently, it was found that selected orphan nuclear receptors in the NR4A family (nerve growth factor-induced-β/NGFI-β), including NR4A1 (Nur77) and NR4A2 (Nurr1), can inhibit the inflammatory effects of NF-κB but there are no approved drugs that target these receptors. In the current studies, we utilized several experimental approaches to target neuroinflammation in cellular models of PD and manganese neurotoxicity in primary glia and in animal models. One of these studies demonstrated that a novel ligand of NR4A1 and NR4A2, 1,1-bis (3'-indolyl) -1-(p-methoxyphenyl) methane (C-DIM5), suppressed NF-κB-dependent inflammatory gene expression in astrocytes following treatment with 1-methyl-4-phenyl-1, 2, 3,6-tetrahydropyridine (MPTP) and the inflammatory cytokines, IFN-γ and TNF-α. These data were further supported by previous studies from our laboratory, which examined efficacy of multiple C-DIM compounds in PD animal and cellular models, including one (C-DIM12) identified as a modulator of Nurr1 activity that also inhibited NF-kB-dependent gene expression in glial cells. Collectively, these data demonstrate that NR4A1/Nur77 and NR4A2/Nurr1 dynamically regulated inflammatory gene expression in glia by modulating the transcriptional activity of NF-κB. An additional study examined the role of NF-κB in manganese (Mn)-induced neurotoxicity by exposing purified microglia, astrocytes (from both wild-type and an astrocyte- specific NF-kB (IKK2) knock-out (KO) mouse) and mixed glial cultures to varying Mn concentrations and then treated neurons with the conditioned media (GCM) of each cell type. In doing so, we showed that mixed glial cultures exposed to Mn enhanced glial activation and neuronal death compared to microglia, wild type astrocytes or IKK2-knockout astrocytes alone or in mixed cultures suggesting that astrocytes are a critical mediator of Mn neurotoxicity through enhanced expression of inflammatory cytokines and chemokines, including those most associated with reactive phenotype such as C3 and CCL2.…
Advisors/Committee Members: Tjalkens, Ronald B. (advisor), Bouma, Gerrit J. (committee member), Goodrich, Laurie R. (committee member), Legare, Marie E. (committee member), McLean, Jennifer L. (committee member).
Subjects/Keywords: neuroinflammation; glia; neuron
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Popichak, K. A. (2018). Glial signaling mechanisms in the progression of neuroinflammatory injury. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/191273
Chicago Manual of Style (16th Edition):
Popichak, Katriana A. “Glial signaling mechanisms in the progression of neuroinflammatory injury.” 2018. Doctoral Dissertation, Colorado State University. Accessed March 04, 2021.
http://hdl.handle.net/10217/191273.
MLA Handbook (7th Edition):
Popichak, Katriana A. “Glial signaling mechanisms in the progression of neuroinflammatory injury.” 2018. Web. 04 Mar 2021.
Vancouver:
Popichak KA. Glial signaling mechanisms in the progression of neuroinflammatory injury. [Internet] [Doctoral dissertation]. Colorado State University; 2018. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/10217/191273.
Council of Science Editors:
Popichak KA. Glial signaling mechanisms in the progression of neuroinflammatory injury. [Doctoral Dissertation]. Colorado State University; 2018. Available from: http://hdl.handle.net/10217/191273

Ruhr Universität Bochum
14.
Diykov, Dmitry.
Changes in GABAergic mechanisms and cation-chloride
co-transports in the albino visual cortex.
Degree: 2008, Ruhr Universität Bochum
URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351
► In der vorliegenden Doktorarbeit konnte zum 1. Mal gezeigt werden, dass in Neuronen des visuellen Cortex albinoter Ratten der Na-K-Cl Kotransporter (NKCC1, Cl- -Aufnahme) im…
(more)
▼ 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
Vergleich zu pigmentierten Ratten überexprimiert wird. Dies
korreliert mit einer gleichzeitigen Verschiebung des
Umkehrpotenzials GABA-vermittelter Cl- -Ströme zu positiveren
Werten. Eine Reduktion des Chlorid-Einwärtstransportes durch
Blockierung des NKCC1 mit Bumetanid oder ähnlicher Pharmaka könnte
die Sehleistung albinoter Tiere verbessern. Zusätzlich wurde die
frühe postnatale Entwicklung des Umkehrpotenzials GABAAR
vermittelter Ströme in Neuronen des visuellen Cortex albinoter und
pigmentierter Ratten verglichen. Zum Zeitpunkt der Geburt wurden
keine Unterschiede gefunden. Zum Zeitpunkt der Augenöffnung (zweite
postnatale Woche) ist in Neuronen des visuellen Cortex albinoter
Ratten das Umkehrpotential GABAAR vermittelter Ströme um 15 mV
postiver und die intrazelluläre Chloridkonzentration
höher.
Advisors/Committee Members: Neuroscience.
Subjects/Keywords: Albinismus; Sehrinde; Aminbuttersäure (gamma-);
Neuron
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Diykov, Dmitry. “Changes in GABAergic mechanisms and cation-chloride
co-transports in the albino visual cortex.” 2008. Thesis, Ruhr Universität Bochum. Accessed March 04, 2021.
http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Diykov, Dmitry. “Changes in GABAergic mechanisms and cation-chloride
co-transports in the albino visual cortex.” 2008. Web. 04 Mar 2021.
Vancouver:
Diykov D. Changes in GABAergic mechanisms and cation-chloride
co-transports in the albino visual cortex. [Internet] [Thesis]. Ruhr Universität Bochum; 2008. [cited 2021 Mar 04].
Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Diykov D. Changes in GABAergic mechanisms and cation-chloride
co-transports in the albino visual cortex. [Thesis]. Ruhr Universität Bochum; 2008. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-22351
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universiteit Utrecht
15.
Goossens, R.
Mechanisms of selective mRNA transport and translation in neuronal axons.
Degree: 2014, Universiteit Utrecht
URL: http://dspace.library.uu.nl:8080/handle/1874/291824
► Selectively targeting mRNA to subcellular locations for local translation allows the distal regions of cells to rapidly respond to extracellular cues. In developing neurons, axons…
(more)
▼ 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 obtain a certain level of autonomy by changing the local proteome in the growth cone during their navigation through the developing nervous system. Studies of mature axons have shown that active local translation still plays an important role in axon maintenance, with evidence suggesting that local translation of mRNA is also indispensible for mounting a sufficient regenerative response upon damage of the axon. Axons seem to gradually lose their local translation abilities as they become more mature, meaning that a thorough understanding of how this ability can be restored could prove beneficial for treating people suffering from damage to their central nervous system. This thesis aims to review literature concerning the mechanisms involved in the selective localization of mRNAs by axoplasmic transport, and will also cover the functionality and regulating factors which induce local translation in the axon.
Advisors/Committee Members: Hoogenraad, C..
Subjects/Keywords: Neuron; axon; mRNA; translation; transport
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Goossens, R. “Mechanisms of selective mRNA transport and translation in neuronal axons.” 2014. Masters Thesis, Universiteit Utrecht. Accessed March 04, 2021.
http://dspace.library.uu.nl:8080/handle/1874/291824.
MLA Handbook (7th Edition):
Goossens, R. “Mechanisms of selective mRNA transport and translation in neuronal axons.” 2014. Web. 04 Mar 2021.
Vancouver:
Goossens R. Mechanisms of selective mRNA transport and translation in neuronal axons. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2021 Mar 04].
Available from: http://dspace.library.uu.nl:8080/handle/1874/291824.
Council of Science Editors:
Goossens R. Mechanisms of selective mRNA transport and translation in neuronal axons. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/291824

University of California – Santa Cruz
16.
Kmet, Muriel Marie.
Differentiation of human embryonic stem cells into Corticofugal projection neurons.
Degree: Molecular Cell and Developmental Biology, 2013, University of California – Santa Cruz
URL: http://www.escholarship.org/uc/item/1jp080qr
► Understanding how neuronal diversity is achieved within the cerebral cortex remains a major challenge in neuroscience. The surge of human embryonic stem cells (hESCs) as…
(more)
▼ 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 a novel model system provides a unique opportunity to study human corticogenesis in vitro and€ identify the mechanisms that promote neuronal differentiation to achieve neuronal diversity in the human brain. Here, we demonstrate the derivation of corticofugal neurons from a genetically engineered Fezf2-YFP hESC reporter line, and uncover two distinct Fezf2 subpopulations that are reminiscent of the 2 Fezf2-expressing neuronal subtypes in the developing mouse brain. Fezf2 is a transcription factor that is both necessary and sufficient for the specification of subcerebral projection neurons in mouse. Its role in human corticogenesis is still unknown. However, the high conservation of FEZF2 protein between mouse and human suggest that Fezf2 is a specific marker of human cerebral neurons as well. Two hypotheses drove our research: 1) Extrinsic factors that modulate in vivo developmental signaling pathways play a critical role in the differentiation of hESCs to a corticofugal fate in vitro; 2) Human embryonic stem cell-derived neurons can survive in vivo and extend axonal projections to specific targets in the rodent brain. Our research shows that hESCs-derived corticofugal neurons are an effective model system to investigate the molecular pathways that regulate human cortical differentiation, axon extension and survival, an endeavor that was until now proscribed due to the manipulation of human embryos.
Subjects/Keywords: Biology; Neurosciences; Fezf2; hESCs; neuron
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Kmet, Muriel Marie. “Differentiation of human embryonic stem cells into Corticofugal projection neurons.” 2013. Thesis, University of California – Santa Cruz. Accessed March 04, 2021.
http://www.escholarship.org/uc/item/1jp080qr.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kmet, Muriel Marie. “Differentiation of human embryonic stem cells into Corticofugal projection neurons.” 2013. Web. 04 Mar 2021.
Vancouver:
Kmet MM. Differentiation of human embryonic stem cells into Corticofugal projection neurons. [Internet] [Thesis]. University of California – Santa Cruz; 2013. [cited 2021 Mar 04].
Available from: http://www.escholarship.org/uc/item/1jp080qr.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kmet MM. Differentiation of human embryonic stem cells into Corticofugal projection neurons. [Thesis]. University of California – Santa Cruz; 2013. Available from: http://www.escholarship.org/uc/item/1jp080qr
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Tasmania
17.
Blizzard, CA.
The response of the mature central nervous system to traumatic brain injury
.
Degree: 2011, University of Tasmania
URL: https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf
;
https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf
► The mature central nervous system (CNS) is unable to repair following traumatic brain injury (TBI). Intervention is difficult as the pathobiology of the brain following…
(more)
▼ The mature central nervous system (CNS) is unable to repair following traumatic brain
injury (TBI). Intervention is difficult as the pathobiology of the brain following injury is
a complex sequence of events that needs to be fully elucidated. Understanding the
endogenous mechanisms evoked by the damaged brain when attempting repair from
injury is vital for devising effective therapies to treat brain injury. The current thesis is
based upon the hypotheses that ultimately, recovery following trauma will require the
induction of neurogenesis and either appropriate regeneration or compensatory
plasticity of pre-existing neural pathways and that the mechanisms underlying
regeneration of mature axons is fundamentally different to developmental growth.
This thesis investigated the reactive and regenerative alterations associated with the
neural response to physical injury in the adult mammalian brain. This thesis studies are
focused upon the potential for regeneration following injury and how comparable
regenerating neurons characteristics are to their developmental counterparts. It
investigated the alterations within the damaged neurons and the surrounding brain area
which may be indicative of an intrinsic capacity for regeneration including frank
neuronal replacement following injury, and the role of the neuronal cytoskeleton in
neuronal regenerative events, as the mechanisms underlying these processes are
currently poorly understood.
This thesis demonstrated that heterogenous populations of cultured cortical neurons are
able to survive and regenerate following severe structural injury, suggesting that
neurons have an intrinsic capacity for regeneration, regardless of the mode of injury.
Additionally, alteration of the intrinsic cytoskeletal environment, through the knockout
of the neurofilament light chain protein, decreased the regenerative ability of mature
neurons, providing further evidence for the intrinsic regulation of regeneration. Results
from this thesis indicate that the growth cones of regenerative sprouts differ from their
developmental counterparts in their predominant morphology, their dynamic behaviour
and their ability to respond to critical growth factors. These differences between the
regenerating and developing growth cones may account for the inability of regenerative sprouting axons to make accurate pathway decisions and successfully respond to
trauma.
The presence of neurogenesis was investigated following structural injury in vitro,
which indicated no evidence of neurogenesis following injury. While focal brain injury
in vivo induced proliferation of neural progenitors, immunohistochemistry confirmed
that astrocytic but not neuronal, cell proliferation was evoked by focal injury, consistent
with the in vitro data. However focal injury induced an axonal regenerative response
into the injury site, which was neuronal cell type specific, and significant remodelling in
a subpopulation of interneurons away from the injury, demonstrating that the adult
cortex is…
Subjects/Keywords: brain; injury; CNS; neuron; regeneration
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Blizzard, CA. “The response of the mature central nervous system to traumatic brain injury
.” 2011. Thesis, University of Tasmania. Accessed March 04, 2021.
https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Blizzard, CA. “The response of the mature central nervous system to traumatic brain injury
.” 2011. Web. 04 Mar 2021.
Vancouver:
Blizzard C. The response of the mature central nervous system to traumatic brain injury
. [Internet] [Thesis]. University of Tasmania; 2011. [cited 2021 Mar 04].
Available from: https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Blizzard C. The response of the mature central nervous system to traumatic brain injury
. [Thesis]. University of Tasmania; 2011. Available from: https://eprints.utas.edu.au/12271/1/Whole-C.Blizzard.PhDThesis.pdf ; https://eprints.utas.edu.au/12271/2/C.BlizzardFigures.pdf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University
18.
Clanton, Joshua Aaron.
Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.
Degree: PhD, Biological Sciences, 2013, Vanderbilt University
URL: http://hdl.handle.net/1803/10639
► Parapineal precursors arise from the medially located pineal complex anlage and migrate to the left side of the brain. Published data implicates Fgf8a in the…
(more)
▼ 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 migration of parapineal cells away from the midline of the pineal anlage. However, the potential role for Fgf8a during the acquisition of parapineal cell fate was not addressed. We have found that Fgf8a regulates a fate decision among specified parapineal precursors that occurs just prior to the initiation of leftward migration. Attenuation of Fgf signaling results in the loss of parapineal cells and the gain of additional cone cells. Data obtained from the combined loss of Flh and Fgf8a, as well as cell fate analysis, shows that in the absence of Fgf signaling, parapineal precursors differentiate as cone photoreceptors rather than parapineal cells. Furthermore, Fgf8a acts permissively to promote parapineal fate in conjunction with the transcription factor Tbx2b, but acts by itself to either block cone photoreceptor fate or promote parapineal differentiation. This cell fate change is independent of Bmp signaling, which promotes the formation of pineal photoreceptors. Instead, parapineal cell differentiation likely requires the two transcription factors, Lhx2b and Lhx9, which are responsive to Fgf signaling and are involved in parapineal formation.
Advisors/Committee Members: James G. Patton (committee member), Jason R. Jessen (committee member), Michael K. Cooper (committee member), Joshua T. Gamse (committee member), Douglas G. McMahon (Committee Chair).
Subjects/Keywords: Left-right asymmetry; neuron; Differentiation
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Clanton, J. A. (2013). Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10639
Chicago Manual of Style (16th Edition):
Clanton, Joshua Aaron. “Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021.
http://hdl.handle.net/1803/10639.
MLA Handbook (7th Edition):
Clanton, Joshua Aaron. “Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish.” 2013. Web. 04 Mar 2021.
Vancouver:
Clanton JA. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1803/10639.
Council of Science Editors:
Clanton JA. Fgf Signaling Governs the Differentiation of Parapineal Neurons in Zebrafish. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/10639

Penn State University
19.
Ma, Ningxin.
TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION.
Degree: 2019, Penn State University
URL: https://submit-etda.libraries.psu.edu/catalog/16624nxm31
► Reprogramming of astrocytes into neurons represents a promising approach to regenerate new neurons for brain repair, but the underlying mechanisms driving this trans-differentiation process are…
(more)
▼ Reprogramming of astrocytes into neurons represents a promising approach to regenerate new neurons for brain repair, but the underlying mechanisms driving this trans-differentiation process are not well understood. In previous work, we have demonstrated that astrocytes can be effectively reprogrammed into functional neurons in two ways. The ectopic expression of a single transcription factor NeuroD1 converted reactive astrocytes into neurons both in vitro and in vivo. Moreover, we recently identified four small molecules - CHIR99021, DAPT, LDN193189 and SB431542 - that could reach highly efficient neuronal conversion in cultured human fetal astrocytes.
Here we employ the next generation of RNA-sequencing technology to investigate the transcriptome changes during the astrocyte-to-
neuron (AtN) conversion process. The four small molecules together can rapidly activate the hedgehog signaling pathway while downregulating many glial genes such as FN1 and MYL9 within 24 hours of treatment. Chemical reprogramming is mediated by several waves of differential gene expression, including upregulation of hedgehog, Wnt/β- catenin, and Notch signaling pathways, together with downregulation of TGF-β and JAK/STAT signaling pathways. Co-expression gene network analyses identify functional gene modules that may directly respond to chemical treatment. In addition, we reveal many well-connected hub genes such as RGMA, neuronatin (NNAT), neurogenin 2 (NEUROG2), NPTX2, MOXD1, JAG1, and GAP43, which may coordinate the chemical reprogramming process.
In comparison to chemical administration, use of virus triggers strong inflammation- related gene expression and impedes cell cycle. With a more than 100-fold increase by virus, NeuroD1 also directly upregulate its target genes, including neurotransmitter receptors, MAPK and cAMP signaling pathways. Moreover, network analyses suggest significant NeuroD1-correlated genes such as CABP7 and LRRTM2, and also indicate the extensive interactions between neurogenic genes (e.g. SOX13, NEUROD6) and glial genes (e.g. HHEX, PRDM1). Together, these findings provide critical insights into the molecular cascades triggered by either a combination of small molecules or a proneural transcription factor, and depict a trajectory that gradually reprogram astrocytes into neurons. Understanding the molecular mechanisms of cell fate determination during chemical or transcription factor-mediated reprogramming will be instrumental for further development of an efficient clinical application in the future.
Advisors/Committee Members: Gong Chen, Dissertation Advisor/Co-Advisor, Gong Chen, Committee Chair/Co-Chair, Yingwei Mao, Committee Member, Shaun Mahony, Committee Member, Qunhua Li, Outside Member.
Subjects/Keywords: reprogramming; astrocyte; neuron; RNA sequencing
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ma, N. (2019). TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/16624nxm31
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ma, Ningxin. “TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION.” 2019. Thesis, Penn State University. Accessed March 04, 2021.
https://submit-etda.libraries.psu.edu/catalog/16624nxm31.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ma, Ningxin. “TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION.” 2019. Web. 04 Mar 2021.
Vancouver:
Ma N. TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION. [Internet] [Thesis]. Penn State University; 2019. [cited 2021 Mar 04].
Available from: https://submit-etda.libraries.psu.edu/catalog/16624nxm31.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ma N. TRANSCRIPTOME ANALYSIS OF DIRECT ASTROCYTE-TO-NEURON CONVERSION. [Thesis]. Penn State University; 2019. Available from: https://submit-etda.libraries.psu.edu/catalog/16624nxm31
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Debrecen
20.
Papp, Zsuzsanna.
Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata
.
Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2010, University of Debrecen
URL: http://hdl.handle.net/2437/95968
► A nucleus cochlearis (CN) a hallópálya els4 átkapcsolódási helye, melyben az elágazó hallóidegrostok többféle neurontípussal létesítenek szinaptikus kapcsolatot (pl. óriás-, piramis-, Purkinje-szer<- és cartwheel-sejtek). Bár…
(more)
▼ A nucleus cochlearis (CN) a hallópálya els4 átkapcsolódási helye, melyben az elágazó
hallóidegrostok többféle neurontípussal létesítenek szinaptikus kapcsolatot (pl. óriás-, piramis-,
Purkinje-szer<- és cartwheel-sejtek). Bár az egyes sejttípusok általában jól elkülöníthet4k
egymástól, bizonyos esetekben komoly nehézségekbe ütközhet az egyértelm< sejtazonosítás.
A jelen munka célja a CN két jellegzetes neurontípusának (óriás- és cartwheel-sejtek), és azok
nyúlványrendszerének morfometriai jellemzése, és az így nyert paraméterek összehasonlítása
volt. A morfometriai analízis végzésére az elektrofiziológiai méréseink során biocitinnel
feltöltött sejteket alkalmaztunk, amiket streptavidinnel konjugált Alexa-488 fluorofórral
tettünk láthatóvá. Az így „el4hívott” sejtekr4l konfokális mikroszkópos optikai rétegfelvételsorozatot
készítettünk (ún. „Z-stack” üzemmód), amikb4l a „NeuronStudio” program
segítségével elkészítettük a kérdéses neuronok ún. „térfogati modelljét”. A modell
segítségével az egyes sejtek nyúlványrendszerének elágazódását számszer<síthet4 morfológia
paraméterekkel tudtuk jellemezni. A sejtek morfológiai leírásánál kiindulási paraméterekként a
szóma legnagyobb és legkisebb átmér4jét, a sejttestb4l induló nyúlványok számát, a
nyúlványrendszer egészének legnagyobb átmér4jét, és a legnagyobb átmér4re mer4leges
maximális átmér4jét határoztuk meg. A sejtek nyúlványrendszerének elágazódottságát részben
az egész nyúlványrendszert jellemz4 paraméterekkel, részben az elágazódási rendeket jellemz4
paraméterekkel, továbbá Sholl-analízissel és polárhisztogramm-analízissel igyekeztünk
jellemezni. Reményeink szerint a fenti paraméterek konzekvens és pontosan dokumentált
meghatározásával mód nyílhat a DCN neuronoknak az eddigieknél pontosabb, a funkcionális
sajátságokkal nagyobb mérték< harmóniát mutató morfológiai csoportosítására. Ezt támasztja
alá azon megfigyelésünk, ami szerint a fenti paraméterek közül némelyekben jelent4s
különbséget mutattunk ki a vizsgált két sejttípus között, ami megkönnyítheti ezen
neuronféleségek pontos klasszifikálását.
Advisors/Committee Members: Rusznák, Zoltán (advisor).
Subjects/Keywords: neuron;
nucleus cochlearis;
morfológia
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Papp, Zsuzsanna. “Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata
.” 2010. Thesis, University of Debrecen. Accessed March 04, 2021.
http://hdl.handle.net/2437/95968.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Papp, Zsuzsanna. “Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata
.” 2010. Web. 04 Mar 2021.
Vancouver:
Papp Z. Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata
. [Internet] [Thesis]. University of Debrecen; 2010. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/2437/95968.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Papp Z. Patkány nucleus cochlearis dorsalis neuronjainak morfológiai vizsgálata
. [Thesis]. University of Debrecen; 2010. Available from: http://hdl.handle.net/2437/95968
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

George Mason University
21.
Graybeal, Lacey.
The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons
.
Degree: 2014, George Mason University
URL: http://hdl.handle.net/1920/9097
► Dendrites serve as the primary sites for synaptic and sensory neuronal input and impairments in dendrite morphogenesis can result in various neurological diseases such as…
(more)
▼ Dendrites serve as the primary sites for synaptic and sensory neuronal input and impairments in dendrite morphogenesis can result in various neurological diseases such as Rett, Down, and Fragile X Syndromes (Kaufmann & Moser, 2000). Thus, uncovering the cellular and molecular mechanisms that govern dendritogenesis in various neurons is important for advancing our understanding of these diseases. Macroautophagy (hereafter referred to as ‘autophagy’) has emerged as a topic of interest in this area, as postmitotic neurons are known to require high basal autophagy in terms of clearing misfolded and/or damaged organelles. Moreover, defects in basal autophagy have been directly linked to neurodegeneration, including neuronal cell death, axon degeneration, and aberrant synapase development which suggests that autophagy has a neuroprotective function (Shen & Ganetzky, 2009; Wong & Cuervo, 2010; Yang, Coleman, Zhang, Zheng, & Yue, 2013). However, despite a well documented role for autophagy in neuronal survival and axonal development, little is known regarding the role of basal autophagy in mediating dendritic arborization or the mechanisms by which the autophagy pathway may be transcriptionally regulated to mediate differential dendritic homeostasis. Thus, we have investigated these mechanisms by utilizing dendritic arborization (da) neurons in the Drosophila melanogaster peripheral nervous system (PNS), which serve as a powerful model for investigating class specific molecular mechanisms of dendrite development and maintenance (Corty, Matthews, & Grueber, 2009; Jan & Jan, 2010). Preliminary microarray analyses demonstrate that the homeodomain transcription factor Cut positively regulates expression of autophagy related genes (Atg) in da neurons. Due to the native differential expression of Cut across the four da
neuron subclasses correlating with distinct levels of dendritic complexity (CI-IV) (Grueber, Jan, & Jan, 2002), the central hypothesis of the studies described herein is that Cut differentially regulates the autophagy pathway as a key mechanism in mediating class specific dendritic homeostasis. By utilizing a combination of in vivo genetics, live confocal microscopy, gene expression analysis, immunohistochemistry, and quantitative neuromorphometry, we investigated the role of basal autophagy in regulating class specific dendrite morphogenesis.
Here we establish that basal autophagy is required to promote normal class specific dendrite morphogenesis and that it exerts differential effects across da
neuron subclasses. We also demonstrate that key autophagy genes (Atg) are positively regulated, in part, by the transcription factor Cut, and that basal autophagy plays a neuroprotective role in regulating higher order dendritic complexity in neurons expressing Cut, namely CIII and CIV da neurons. Cut-independent effects were also observed in the relatively simple CI neurons, where basal autophagy functions to constrain dendritic arbors. Autophagic dysregulation through loss-of-function (LOF) and gain-of-function (GOF)…
Advisors/Committee Members: Cox, Daniel N (advisor).
Subjects/Keywords: dendrite;
neuron;
autophagy;
morphogenesis;
Drosophila
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Graybeal, Lacey. “The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons
.” 2014. Thesis, George Mason University. Accessed March 04, 2021.
http://hdl.handle.net/1920/9097.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Graybeal, Lacey. “The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons
.” 2014. Web. 04 Mar 2021.
Vancouver:
Graybeal L. The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons
. [Internet] [Thesis]. George Mason University; 2014. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1920/9097.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Graybeal L. The Role of Basal Autophagy in Regulating Class Specific Dendrite Morphogenesis in Drosophila Sensory Neurons
. [Thesis]. George Mason University; 2014. Available from: http://hdl.handle.net/1920/9097
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto
22.
Jiang, Ke.
The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration.
Degree: 2013, University of Toronto
URL: http://hdl.handle.net/1807/70090
► Inherited photoreceptor degeneration (IPD) is characterized by progressive death of mutant photoreceptors (PRs). To date, mutations in over 186 genes have been associated with IPD.…
(more)
▼ Inherited photoreceptor degeneration (IPD) is characterized by progressive death of mutant photoreceptors (PRs). To date, mutations in over 186 genes have been associated with IPD. Unfortunately, little progress has been made towards treatment to prevent PR death. Here I show that expression of the signal transducer and activator of transcription 3 (STAT3) is increased and activated by tyrosine phosphorylation in both PRs and Müller glia of three mouse models of IPD (Tg(RHO P347S), Prph2rds+/- and Pde6brd1/rd1). To determine whether this endogenous activation of Stat3 expression influence PR degeneration, I genetically manipulated Stat3 expression in these two cell types in three IPD models. PR-specific deletion of Stat3 significantly accelerated PR death in Tg(RHO P347S) and Prph2rds+/- retinas. These data revealed, for the first time, that the increased expression of endogenously activated PR-STAT3 is a survival response in mutant PRs. Accordingly, increases in Stat3 expression may form the basis of a PR protective therapy in IPDs. To examine this hypothesis, I transgenically expressed various Stat3 alleles specifically in the PRs of wild type and IPD mice. The expression of a wild type Stat3 allele or a constitutively active Stat3 allele (Stat3C) in the PRs increased their survival in Tg(RHO P347S) mice at PN30 and in Prph2rds+/- mice at 6 months. Phosphorylation of STAT3 at tyrosine 705 was required for the pro-survival effect as the introduction of a Stat3Y705F allele was not protective. Unexpectedly, the deletion of Stat3 from PRs of Pde6brd1/rd1 mice improved PR survival. The basis for this contrasting result is unclear. However, as with the other two IPD models, PR survival was increased with expression of wild type Stat3 or Stat3C alleles in the PRs of Pde6brd1/rd1 mice. When Stat3 was deleted specifically in Müller glial cells in Prph2rds+/- retinas, a small but significant increase in PR survival was observed at 6 months of age, suggesting that the increased expression of Stat3 in Müller glial in IPDs may be pathogenetic. In summary, I have demonstrated that the increased expression and activation of STAT3 is a survival response in mammalian IPDs, a finding with important therapeutic implications for human retinal degenerations.
PhD
Advisors/Committee Members: McInnes, Roderick, Molecular and Medical Genetics.
Subjects/Keywords: Retina; Photoreceptor; Neuron death; 0317
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jiang, K. (2013). The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/70090
Chicago Manual of Style (16th Edition):
Jiang, Ke. “The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration.” 2013. Doctoral Dissertation, University of Toronto. Accessed March 04, 2021.
http://hdl.handle.net/1807/70090.
MLA Handbook (7th Edition):
Jiang, Ke. “The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration.” 2013. Web. 04 Mar 2021.
Vancouver:
Jiang K. The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration. [Internet] [Doctoral dissertation]. University of Toronto; 2013. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1807/70090.
Council of Science Editors:
Jiang K. The Role of Stat3 in Mouse Models of Inherited Photoreceptor Degeneration. [Doctoral Dissertation]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/70090

University of New Mexico
23.
Bird, Clark.
The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons.
Degree: Biomedical Sciences Graduate Program, 2012, University of New Mexico
URL: https://digitalrepository.unm.edu/biom_etds/65
► The KH-type splicing regulatory protein (KSRP) promotes the decay of AU-rich element (ARE) containing mRNAs. Although KSRP is expressed in the developing and mature nervous…
(more)
▼ 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 system, very little is known about its role in regulating gene expression in the brain. In this study, we utilized in vitro binding and decay studies to examine whether KSRP regulates the stability of the GAP-43 transcript, an ARE-containing neuronal mRNA whose protein product plays a role in axonal growth and synaptic plasticity. We found KSRP destabilizes GAP-43 mRNA by binding to the GAP-43 ARE, a process that depends on the presence of the fourth KH domain in the protein. Furthermore, KSRP competed with another GAP-43 mRNA binding protein, the stabilizing factor HuD, for binding to these ARE sequences. Given that GAP-43 expression is crucial for accurate axonal outgrowth during neuronal development, we also examined the functional consequences of KSRP overexpression and depletion on the axonal outgrowth from primary hippocampal neurons. Overexpression of either full length KSRP or KSRP without the nuclear localization signal hindered axonal outgrowth in these cultures, while overexpression of a mutant protein without the KH4 domain did not have any effect. In contrast, depletion of KSRP led to a dramatic increase in axonal length. Concurrent overexpression of GAP-43 and KSRP rescued the axonal outgrowth deficits seen with KSRP overexpression, but only when the GAP-43 mRNA was targeted to axons using GAP-43 or amphoterin 3 UTR sequences. Together, our results suggest that KSRP is an important regulator of GAP-43 mRNA stability and neuronal differentiation that works in direct opposition to HuD.
Advisors/Committee Members: Perrone-Bizzozero, Nora, Valenzuela, Fernando, Caldwell, Kevin, Hartley, Rebecca.
Subjects/Keywords: GAP-43; KSRP; Neuron outgrowth
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Bird, Clark. “The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons.” 2012. Doctoral Dissertation, University of New Mexico. Accessed March 04, 2021.
https://digitalrepository.unm.edu/biom_etds/65.
MLA Handbook (7th Edition):
Bird, Clark. “The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons.” 2012. Web. 04 Mar 2021.
Vancouver:
Bird C. The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons. [Internet] [Doctoral dissertation]. University of New Mexico; 2012. [cited 2021 Mar 04].
Available from: https://digitalrepository.unm.edu/biom_etds/65.
Council of Science Editors:
Bird C. The RNA binding protein KSRP destabilizes GAP-43 mRNA to limit axonal elongation in cultured hippocampal neurons. [Doctoral Dissertation]. University of New Mexico; 2012. Available from: https://digitalrepository.unm.edu/biom_etds/65

University of Iowa
24.
Ulrich, Jason Daniel.
The regulaton and function of nuclear factor of activated T-cells in neurons.
Degree: PhD, Pharmacology, 2011, University of Iowa
URL: https://ir.uiowa.edu/etd/2782
► Ca2+-dependent transcription is a fundamental process by which neurons translate activation experience into cellular level adaptations. The nuclear factor of activated T-cells (NFAT) family…
(more)
▼ Ca2+-dependent transcription is a fundamental process by which neurons translate activation experience into cellular level adaptations. The nuclear factor of activated T-cells (NFAT) family of proteins comprise four Ca2+/CaN-dependent transcription factors that are widely expressed throughout virtually all tissues. Within neurons, NFAT dependent signaling is critical for axonal development, regulation of synapse number and efficacy, and survival. Furthermore, NFAT is implicated in activity dependent regulation of genes involved in synaptic transmission, learning and memory, mood, and pain sensation. NFAT is activated upon elevations in intracellular Ca2+, which results in CaN -dependent dephosphorylation of multiple serine residues within an N-terminal regulatory region. NFAT dephosphorylation permits NFAT translocation to the nucleus, where it can regulate gene expression, frequently co-operatively with other transcription factors, including AP-1 and MEF2. NFAT activation is opposed or terminated by several kinases, including CK1 and GSK3. Despite the importance of NFAT proteins as regulators of Ca2+-dependent transcription, little is known about the regulation and function of specific NFAT isoforms within neurons. In Aim 1 of this thesis I characterized the differential activation of NFATc3 and NFATc4 in DRG neurons. While NFATc3 rapidly translocates the nucleus upon Ca2+-influx through voltage-gated calcium channels, NFATc4 remained remarkably intransient. Modular substitution of NFATc3 regulatory elements increased the rate or retention of NFATc4, whereas converse substitutions of NFATc4 regulatory elements into NFATc3 decreased NFATc3 nuclear translocation. The activation of NFATc4 appears to be inhibited by preferential phosphorylation by kinases, such as GSK3, which counteract CaN-dependent dephosphorylation. In Aim 2 I investigated the role of NFATc3 in hippocampal neurons. While the majority of NFAT reports in neurons have focused on NFATc4, my data suggest that NFATc3 is the predominantly expressed isoform in hippocampal neurons and is critical for depolarization-induced NFAT target gene expression. I further characterized NFATc3 KO mice in a battery of behavioral assays to test whether loss of NFATc3 expression would affect the baseline anxiety/depression state of the animal, or if NFATc3 was critical for learning and memory. Taken together, my data suggest that NFATc3 is important for NFAT-dependent gene expression in central and peripheral neurons and that distinct regulation of NFAT isoforms within neurons may underlie isoform-specific effects on gene expression.
Advisors/Committee Members: Usachev, Yuriy M. (supervisor).
Subjects/Keywords: Calcium; Neuron; NFAT; Transcription; Pharmacology
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APA (6th 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 (16th Edition):
Ulrich, Jason Daniel. “The regulaton and function of nuclear factor of activated T-cells in neurons.” 2011. Doctoral Dissertation, University of Iowa. Accessed March 04, 2021.
https://ir.uiowa.edu/etd/2782.
MLA Handbook (7th Edition):
Ulrich, Jason Daniel. “The regulaton and function of nuclear factor of activated T-cells in neurons.” 2011. Web. 04 Mar 2021.
Vancouver:
Ulrich JD. The regulaton and function of nuclear factor of activated T-cells in neurons. [Internet] [Doctoral dissertation]. University of Iowa; 2011. [cited 2021 Mar 04].
Available from: https://ir.uiowa.edu/etd/2782.
Council of Science Editors:
Ulrich JD. The regulaton and function of nuclear factor of activated T-cells in neurons. [Doctoral Dissertation]. University of Iowa; 2011. Available from: https://ir.uiowa.edu/etd/2782

University of Southern California
25.
Mora, Rudy J.
Genetically-encoded probes for visualizing protein
trafficking dynamics in living neurons.
Degree: PhD, Neuroscience, 2012, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015
► Here I describe the development of genetically-encoded probes for visualizing the trafficking of neuronal proteins in living cells. The probes are derived from a diverse…
(more)
▼ 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 library of
small fibronectin domains that resemble antibodies with the
advantage of containing no disulfide bridges which facilitates
proper expression and folding inside cells. Using the directed
evolution technique mRNA display I selected fibronectins that
specifically label the voltage-gated potassium channel Kv4.2
auxiliary subunit KChIP and Ca2+/Calmodulin-dependent Kinase II
(CaMKII) α, proteins both involved in the regulation of long-term
potentiation. As a fusion to GFP the CaMKIIα probe reveals the
rapid translocation of kinase to post-synaptic densities upon
excitatory stimulation. It also reveals a hitherto unreported
localization pattern of large kinase clusters in the cell body.
These cell body CaMKIIα clusters rapidly and reversibly disperse
upon excitatory stimulation in a Ca2+-dependent manner and may
represent a new mechanism by which neurons localize inactive
CaMKIIα. These Fibronectin intrabodies generated by RNA display
(FingRs) combine the advantages of recombinant DNA such as
fluorescent fusion tags with the ability to visualize endogenous
proteins. This technology is a leap forward in visualizing the
trafficking dynamics of native proteins in living
cells.
Advisors/Committee Members: Arnold, Donald B. (Committee Chair), Butler, Samantha (Committee Member), Liman, Emily (Committee Member), Roberts, Richard W. (Committee Member).
Subjects/Keywords: probe; calcium; traffic; neuron; CaMKII
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Mora, R. J. (2012). Genetically-encoded probes for visualizing protein
trafficking dynamics in living neurons. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015
Chicago Manual of Style (16th Edition):
Mora, Rudy J. “Genetically-encoded probes for visualizing protein
trafficking dynamics in living neurons.” 2012. Doctoral Dissertation, University of Southern California. Accessed March 04, 2021.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015.
MLA Handbook (7th Edition):
Mora, Rudy J. “Genetically-encoded probes for visualizing protein
trafficking dynamics in living neurons.” 2012. Web. 04 Mar 2021.
Vancouver:
Mora RJ. Genetically-encoded probes for visualizing protein
trafficking dynamics in living neurons. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Mar 04].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015.
Council of Science Editors:
Mora RJ. Genetically-encoded probes for visualizing protein
trafficking dynamics in living neurons. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/8143/rec/3015

University of Tennessee – Knoxville
26.
Weiss, Ryan John.
Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems.
Degree: MS, Electrical Engineering, 2017, University of Tennessee – Knoxville
URL: https://trace.tennessee.edu/utk_gradthes/4986
► Neuromorphic electronics studies the physical realization of neural networks in discrete circuit components. Hardware implementations of neural networks take advantage of highly parallelized computing power…
(more)
▼ 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 with low energy systems. The hardware designed for these systems functions as a low power, low area alternative to computer simulations. With on-line learning in the system, hardware implementations of neural networks can further improve their solution to a given task.In this work, the analog computational system presented is the computational core for running a spiking neural network model. This component of a neural network, the
neuron, is one of the building blocks used to create neural networks. The
neuron takes inputs from the connected synapses, which each store a weight value. The inputs are stored in the
neuron and checked against a threshold. The
neuron activates, causing a firing event, when the neuron’s internal storage crosses its threshold. The
neuron designed is an Axon-Hillock
neuron utilizing memristive synapses for low area and energy operation.
Advisors/Committee Members: Garrett S. Rose, Benjamin J. Blalock, Mark E. Dean.
Subjects/Keywords: Neuromorphic; Neuron; Memristor; Analog
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Weiss, Ryan John. “Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems.” 2017. Thesis, University of Tennessee – Knoxville. Accessed March 04, 2021.
https://trace.tennessee.edu/utk_gradthes/4986.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Weiss, Ryan John. “Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems.” 2017. Web. 04 Mar 2021.
Vancouver:
Weiss RJ. Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems. [Internet] [Thesis]. University of Tennessee – Knoxville; 2017. [cited 2021 Mar 04].
Available from: https://trace.tennessee.edu/utk_gradthes/4986.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Weiss RJ. Analog Axon Hillock Neuron Design for Memristive Neuromorphic Systems. [Thesis]. University of Tennessee – Knoxville; 2017. Available from: https://trace.tennessee.edu/utk_gradthes/4986
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Tech
27.
Bilodeau, Gregory Peter.
Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells.
Degree: MS, Computer Science and Applications, 2013, Virginia Tech
URL: http://hdl.handle.net/10919/23328
► This paper provides a fully automated method of finding high-quality seed points in 3D space from a stack of images of neuron cells. These seed…
(more)
▼ 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 points may then be used as initial starting points for automated local tracing algorithms, removing a time consuming required user interaction in current methodologies. Methods to collapse the search space and provide rudimentary topology estimates are also presented.
Advisors/Committee Members: Egyhazy, Csaba J. (committeechair), Kulczycki, Gregory W. (committee member), Chen, Ing Ray (committee member).
Subjects/Keywords: Neuron tracing; DIADEM; image analysis
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th Edition):
Bilodeau, Gregory Peter. “Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells.” 2013. Masters Thesis, Virginia Tech. Accessed March 04, 2021.
http://hdl.handle.net/10919/23328.
MLA Handbook (7th Edition):
Bilodeau, Gregory Peter. “Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells.” 2013. Web. 04 Mar 2021.
Vancouver:
Bilodeau GP. Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells. [Internet] [Masters thesis]. Virginia Tech; 2013. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/10919/23328.
Council of Science Editors:
Bilodeau GP. Automated Seed Point Selection in Confocal Image Stacks of Neuron Cells. [Masters Thesis]. Virginia Tech; 2013. Available from: http://hdl.handle.net/10919/23328

University of New South Wales
28.
Curthoys, Nikki Margarita.
Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation.
Degree: Medical Sciences, 2011, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/51454
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true
► The actin cytoskeleton is crucial for many functions including cell motility, cytokinesis, and vesicle formation. Tropomyosins (Tm) are actin associated proteins which regulate the functional…
(more)
▼ The actin cytoskeleton is crucial for many functions including cell motility, cytokinesis, and vesicle formation. Tropomyosins (Tm) are actin associated proteins which regulate the functional capacity of actin filaments. At least 40 Tm isoforms are produced from four genes (αTm, βTm, γTm, and δTm), with differential expression and localisation in tissues, cells and subcellular compartments. As some Tms are potential targets for anti-cancer therapies, one aim of this project was to measure how eliminating one subset of isoforms affected expression of other Tms in brain. Using a knockout (KO) mouse model lacking the γTm-gene 9d exon, regional distributions of Tms were investigated by Western blotting in wild type and 9d KO adult mouse Whole Brain, Cerebellum, Amygdala, Hypothalamus, Cerebral Cortex, Hippocampus, and Olfactory Bulb. KO of γTm-gene isoforms Tm5NM1 and Tm5NM2 was shown to induce upregulation of other γTm-gene products. Regional expression patterns of other Tms, including the δTm-gene product Tm4, were established in brain. A previously unidentified product immunoreactive with the Tm4 antibody was observed and characterised as having similar biochemical properties to Tm4; 2D gel electrophoresis indicated Tm4 and this associated product were both post translationally modified. To investigate Tm4 function in neural cells, rat neuroblastoma cells (B35) were stably transfected with a mammalian vector containing the Tm4 gene. These cells were compared with previously developed B35 clones overexpressing the neuronal isoforms: TmBr1, TmBr2, or TmBr3. Using light microscopy it was shown that while overexpression of these isoforms each induced neurite outgrowth, each had highly specific effects on neurite morphology. Analyses of TmBr2 and Tm4 overexpressing B35 cells by fluorescence activated cell sorting indicated these isoforms could significantly affect cell cycle exit. Quantitative proteomics approaches (LC-MS/MS and iTRAQ) identified proteins affected by overexpression of Tm5NM1, TmBr2, TmBr3, or Tm4 isoforms in B35 cells. These data show for the first time that Tms differentially induce changes in the levels of many other proteins, and Tm expression results in isoform specific profiles of other actin binding proteins (ABP). The actin cytoskeleton underpins neurite outgrowth and branching, and these Tms have been identified as regulators of these events and ABP expression.
Advisors/Committee Members: Fath, Thomas, Faculty of Medicine, UNSW, Gunning, Peter, Faculty of Medicine, UNSW.
Subjects/Keywords: Tropomyosin; Actin; Neuron; Cytoskeleton; Differentation
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Curthoys, Nikki Margarita. “Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation.” 2011. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021.
http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true.
MLA Handbook (7th Edition):
Curthoys, Nikki Margarita. “Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation.” 2011. Web. 04 Mar 2021.
Vancouver:
Curthoys NM. Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2021 Mar 04].
Available from: http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true.
Council of Science Editors:
Curthoys NM. Tropomyosins and the actin cytoskeleton in neuronal morphogenesis and differentiation. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51454 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10140/SOURCE02?view=true

King Abdullah University of Science and Technology
29.
Noutsi, Bakiza Kamal.
Correlation between membrane fluidity cellular development and stem cell differentiation.
Degree: Biological and Environmental Sciences and Engineering (BESE) Division, 2016, King Abdullah University of Science and Technology
URL: http://hdl.handle.net/10754/621954
► Cell membranes are made up of a complex structure of lipids and proteins that diffuse laterally giving rise to what we call membrane fluidity. During…
(more)
▼ Cell membranes are made up of a complex structure of lipids and proteins that diffuse laterally giving rise to what we call membrane fluidity. During cellular development, such as neuronal differentiation, cell membranes undergo dramatic structural changes induced by proteins such as ARC and Cofilin among others in the case of synaptic modification. In this study we used the generalized polarization (GP) property of fluorescent probe Laurdan using two-photon microscopy to determine membrane fluidity as a function of time and for various cell lines. A low GP value corresponds to a higher fluidity and a higher GP value is associated with a more rigid membrane. Four different cell lines were monitored such as hN2, NIH3T3, HEK293 and L6 cells. As expected, NIH3T3 cells have more rigid membrane at earlier stages of their development. On the other hand neurons tend to have the highest membrane fluidity early in their development emphasizing its correlation with plasticity and the need for this malleability during differentiation. This study sheds light on the involvement of membrane fluidity during neuronal differentiation and development of other cell lines.
Advisors/Committee Members: Chaieb, Saharoui (advisor), Magistretti, Pierre J. (committee member), Khashab, Niveen M. (committee member), Gratton, Enrico (committee member).
Subjects/Keywords: Neuron; development; stem cell; Differentiation
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Noutsi, B. K. (2016). Correlation between membrane fluidity cellular development and stem cell differentiation. (Thesis). King Abdullah University of Science and Technology. Retrieved from http://hdl.handle.net/10754/621954
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Noutsi, Bakiza Kamal. “Correlation between membrane fluidity cellular development and stem cell differentiation.” 2016. Thesis, King Abdullah University of Science and Technology. Accessed March 04, 2021.
http://hdl.handle.net/10754/621954.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Noutsi, Bakiza Kamal. “Correlation between membrane fluidity cellular development and stem cell differentiation.” 2016. Web. 04 Mar 2021.
Vancouver:
Noutsi BK. Correlation between membrane fluidity cellular development and stem cell differentiation. [Internet] [Thesis]. King Abdullah University of Science and Technology; 2016. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/10754/621954.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Noutsi BK. Correlation between membrane fluidity cellular development and stem cell differentiation. [Thesis]. King Abdullah University of Science and Technology; 2016. Available from: http://hdl.handle.net/10754/621954
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University
30.
Madison, Jennifer Lea.
Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.
Degree: PhD, Pharmacology, 2011, Vanderbilt University
URL: http://hdl.handle.net/1803/12672
► Huntington’s disease is a fatal autosomal dominant neurodegenerative disease caused by an expansion of CAG repeats in the DNA of the Huntingtin gene. The length…
(more)
▼ Huntington’s disease is a fatal autosomal dominant neurodegenerative disease caused by an expansion of CAG repeats in the DNA of the Huntingtin gene. The length of the repeat is inversely related to the age of disease onset, however it only accounts for 60% of the variability in the age of onset. Therefore, other genetic and environmental effects contribute to the remaining 40% in the variability in age of onset. Multiple neurodegenerative diseases exhibit alterations in metal ion homeostasis. Research in our laboratories has demonstrated a disease-toxicant interaction between mutant Huntingtin and manganese exposure in vitro. Manganese is an essential trace metal that is necessary for many physiological processes, including neurotransmitter synthesis. In high levels, manganese can be damaging to the brain. Exposure that leads to this damage is typically encountered in an occupational setting such as when welding, smelting or mining manganese.
The research described in this dissertation is the first to describe the complex gene-environment interactions between mutant Huntingtin and manganese exposure in vivo. The neurochemical and morphological changes identified herein are complex and exhibit both positive and negative effects. My research also identified the earliest evidence for striatal dendritic pathology in YAC128 mice that occur between 13 and 16 weeks postnatal. Additionally, this is the first research to show gender-specific changes in MSN morphology following manganese exposure. These alterations in
neuron morphology were most prevalent when manganese levels were elevated and were not due to differential striatal manganese accumulation.
Taken together, these data lay the groundwork for understanding the gene-environment interaction between mutant Huntingtin and Mn exposure. Future studies will further our understanding of this interaction that may one day lead to therapeutic intervention. These studies also reinforce the need to include animals of both genders in experimentation to further our understanding of disease across both genders.
Advisors/Committee Members: Malcolm J. Avison (committee member), Gregg D. Stanwood (committee member), Aaron B. Bowman (committee member), Michael Aschner (committee member), Eugenia V. Gurevich (Committee Chair).
Subjects/Keywords: neuron morphology; YAC128; manganese; Huntington's disease; medium spiny neuron; neurochemistry
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Madison, J. L. (2011). Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12672
Chicago Manual of Style (16th Edition):
Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021.
http://hdl.handle.net/1803/12672.
MLA Handbook (7th Edition):
Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Web. 04 Mar 2021.
Vancouver:
Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1803/12672.
Council of Science Editors:
Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/12672
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