Relevant bibliographies by topics / Axon development

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Axon development'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Axon development"

1

Peckol, E. L., J. A. Zallen, J. C. Yarrow, and C. I. Bargmann. "Sensory activity affects sensory axon development in C. elegans." Development 126, no. 9 (May 1, 1999): 1891–902. http://dx.doi.org/10.1242/dev.126.9.1891.

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The simple nervous system of the nematode C. elegans consists of 302 neurons with highly reproducible morphologies, suggesting a hard-wired program of axon guidance. Surprisingly, we show here that sensory activity shapes sensory axon morphology in C. elegans. A class of mutants with deformed sensory cilia at their dendrite endings have extra axon branches, suggesting that sensory deprivation disrupts axon outgrowth. Mutations that alter calcium channels or membrane potential cause similar defects. Cell-specific perturbations of sensory activity can cause cell-autonomous changes in axon morphology. Although the sensory axons initially reach their targets in the embryo, the mutations that alter sensory activity cause extra axon growth late in development. Thus, perturbations of activity affect the maintenance of sensory axon morphology after an initial pattern of innervation is established. This system provides a genetically tractable model for identifying molecular mechanisms linking neuronal activity to nervous system structure.
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Whitington, P. M. "The early development of motor axon pathways in the the establishment of the segmental nerves in the." Development 105, no. 4 (April 1, 1989): 715–21. http://dx.doi.org/10.1242/dev.105.4.715.

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This study has identified the first five motor neurones axons out of the segmental nerves in the thoracic and has traced the pathways followed by these axons up divergence into the ganglionic nerve roots. These out axons in a stereotyped sequence over a short to 2% of embryonic development. Motor axons initially contact the dorsal basal lamina and then parallel array just beneath this membrane. At the edge axons diverge into either of two pathways: an anterior corresponding to nerve root 3 which is pioneered by axon to leave the CNS; and a posterior pathway, root 5, which is pioneered by the second motor axon. axon appears to grow circumferentially around the between the body wall and the base of the coxa, while closely associated with the filopodia or axons of the peripheral pioneer neurones. The later motor axons pathways pioneered by these first two axons. A small molecular markers would be sufficient to generate the of axon growth by these early motor neurones and some cues may be used to guide afferent axons into the CNS.
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Johnson, J. Kelly, and V. A. Casagrande. "Prenatal development of axon outgrowth and connectivity in the ferret visual system." Visual Neuroscience 10, no. 1 (January 1993): 117–30. http://dx.doi.org/10.1017/s0952523800003266.

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AbstractThe objective of this study was to determine when the retina, lateral geniculate nucleus (LGN), and striate cortex first send out axons, and first connect with each other, during embryonic development in the ferret. Specifically, we were interested in the timing relationship between axon outgrowth and known temporal patterns of neurogenesis in the LGN and striate cortex. Ferrets (Mustela putorius furo) were selected for study because of their immature developmental state in late gestation and relatively large litters.We examined axon outgrowth from the retina, and anlagen of presumptive LGN and striate cortex between embryonic day 21–30 (E21–E30) using in situ inoculations of two fluorescent lipophilic dyes, Dil and DiA. Dil inoculations were made into the cortex and contralateral thalamus, and DiA inoculations were made into the contralateral eye. Retinal axon termination zones in the diencephalon following the DiA inoculations were used to validate the location of the LGN.Visual cortex and LGN neurogenesis begins at E20 in ferrets. No axon outgrowth could be documented from retina or anlagen of striate cortex and LGN until E24. At E24 some retinal axons reach and cross the chiasm, cortical axons extend some distance within the cortical radiations, and thalamic axons are within the internal capsule. Retinogeniculate, geniculocortical, and corticogeniculate axons extend to their target structures by E27, as evidenced by retrograde labeling in cells of origin.These data suggest that in the ferret retina, and developing LGN and striate cortex, (1) axon outgrowth from each visual area begins within 24-h of each other, after neurogenesis has begun at the source but before it is complete in the target; (2) axons may be generated before parent cell bodies have completed migration; and (3) arriving axons are in a position to influence target structures almost from their inception.
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Goslin, K., and G. Banker. "Experimental observations on the development of polarity by hippocampal neurons in culture." Journal of Cell Biology 108, no. 4 (April 1, 1989): 1507–16. http://dx.doi.org/10.1083/jcb.108.4.1507.

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In culture, hippocampal neurons develop a polarized form, with a single axon and several dendrites. Transecting the axons of hippocampal neurons early in development can cause an alteration of polarity; a process that would have become a dendrite instead becomes the axon (Dotti, C. G., and G. A. Banker. 1987. Nature (Lond.). 330:254-256). To investigate this phenomenon more systematically, we transected axons at varying lengths. The greater the distance of the transection from the soma, the greater the probability for regrowth of the original axon. However, it was not the absolute length of the axonal stump that determined the response to transection, but rather its length relative to the lengths of the cell's other processes. If one process was greater than 10 microns longer than the others, it invariably became the axon regardless of its identity before transection. Conversely, when a cell's processes were nearly equal in length, it was impossible to predict which would become the axon. In these cases, axonal outgrowth began only after a long latency. During this interval, the processes appeared to be in dynamic equilibrium, some growing for short distances while others retracted. When one process exceeded the others by a critical length, it rapidly elongated to become the axon. The establishment of neuronal polarity during normal development may similarly involve an interaction among processes whose identities have not yet been determined. When, by chance, one exceeds the others by a critical length, it becomes specified as the axon.
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Nishikimi, Mitsuaki, Koji Oishi, and Kazunori Nakajima. "Axon Guidance Mechanisms for Establishment of Callosal Connections." Neural Plasticity 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/149060.

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Numerous studies have investigated the formation of interhemispheric connections which are involved in high-ordered functions of the cerebral cortex in eutherian animals, including humans. The development of callosal axons, which transfer and integrate information between the right/left hemispheres and represent the most prominent commissural system, must be strictly regulated. From the beginning of their growth, until reaching their targets in the contralateral cortex, the callosal axons are guided mainly by two environmental cues: (1) the midline structures and (2) neighboring? axons. Recent studies have shown the importance of axona guidance by such cues and the underlying molecular mechanisms. In this paper, we review these guidance mechanisms during the development of the callosal neurons. Midline populations express and secrete guidance molecules, and “pioneer” axons as well as interactions between the medial and lateral axons are also involved in the axon pathfinding of the callosal neurons. Finally, we describe callosal dysgenesis in humans and mice, that results from a disruption of these navigational mechanisms.
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Llobet Rosell, Arnau, and Lukas J. Neukomm. "Axon death signalling in Wallerian degeneration among species and in disease." Open Biology 9, no. 8 (August 2019): 190118. http://dx.doi.org/10.1098/rsob.190118.

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Axon loss is a shared feature of nervous systems being challenged in neurological disease, by chemotherapy or mechanical force. Axons take up the vast majority of the neuronal volume, thus numerous axonal intrinsic and glial extrinsic support mechanisms have evolved to promote lifelong axonal survival. Impaired support leads to axon degeneration, yet underlying intrinsic signalling cascades actively promoting the disassembly of axons remain poorly understood in any context, making the development to attenuate axon degeneration challenging. Wallerian degeneration serves as a simple model to study how axons undergo injury-induced axon degeneration (axon death). Severed axons actively execute their own destruction through an evolutionarily conserved axon death signalling cascade. This pathway is also activated in the absence of injury in diseased and challenged nervous systems. Gaining insights into mechanisms underlying axon death signalling could therefore help to define targets to block axon loss. Herein, we summarize features of axon death at the molecular and subcellular level. Recently identified and characterized mediators of axon death signalling are comprehensively discussed in detail, and commonalities and differences across species highlighted. We conclude with a summary of engaged axon death signalling in humans and animal models of neurological conditions. Thus, gaining mechanistic insights into axon death signalling broadens our understanding beyond a simple injury model. It harbours the potential to define targets for therapeutic intervention in a broad range of human axonopathies.
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Zallen, J. A., S. A. Kirch, and C. I. Bargmann. "Genes required for axon pathfinding and extension in the C. elegans nerve ring." Development 126, no. 16 (August 15, 1999): 3679–92. http://dx.doi.org/10.1242/dev.126.16.3679.

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Over half of the neurons in Caenorhabditis elegans send axons to the nerve ring, a large neuropil in the head of the animal. Genetic screens in animals that express the green fluorescent protein in a subset of sensory neurons identified eight new sax genes that affect the morphology of nerve ring axons. sax-3/robo mutations disrupt axon guidance in the nerve ring, while sax-5, sax-9 and unc-44 disrupt both axon guidance and axon extension. Axon extension and guidance proceed normally in sax-1, sax-2, sax-6, sax-7 and sax-8 mutants, but these animals exhibit later defects in the maintenance of nerve ring structure. The functions of existing guidance genes in nerve ring development were also examined, revealing that SAX-3/Robo acts in parallel to the VAB-1/Eph receptor and the UNC-6/netrin, UNC-40/DCC guidance systems for ventral guidance of axons in the amphid commissure, a major route of axon entry into the nerve ring. In addition, SAX-3/Robo and the VAB-1/Eph receptor both function to prevent aberrant axon crossing at the ventral midline. Together, these genes define pathways required for axon growth, guidance and maintenance during nervous system development.
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Birgbauer, Eric, Stephen F. Oster, Christophe G. Severin, and David W. Sretavan. "Retinal axon growth cones respond to EphB extracellular domains as inhibitory axon guidance cues." Development 128, no. 15 (August 1, 2001): 3041–48. http://dx.doi.org/10.1242/dev.128.15.3041.

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Axon pathfinding relies on cellular signaling mediated by growth cone receptor proteins responding to ligands, or guidance cues, in the environment. Eph proteins are a family of receptor tyrosine kinases that govern axon pathway development, including retinal axon projections to CNS targets. Recent examination of EphB mutant mice, however, has shown that axon pathfinding within the retina to the optic disc is dependent on EphB receptors, but independent of their kinase activity. Here we show a function for EphB1, B2 and B3 receptor extracellular domains (ECDs) in inhibiting mouse retinal axons when presented either as substratum-bound proteins or as soluble proteins directly applied to growth cones via micropipettes. In substratum choice assays, retinal axons tended to avoid EphB-ECDs, while time-lapse microscopy showed that exposure to soluble EphB-ECD led to growth cone collapse or other inhibitory responses. These results demonstrate that, in addition to the conventional role of Eph proteins signaling as receptors, EphB receptor ECDs can also function in the opposite role as guidance cues to alter axon behavior. Furthermore, the data support a model in which dorsal retinal ganglion cell axons heading to the optic disc encounter a gradient of inhibitory EphB proteins which helps maintain tight axon fasciculation and prevents aberrant axon growth into ventral retina. In conclusion, development of neuronal connectivity may involve the combined activity of Eph proteins serving as guidance receptors and as axon guidance cues.
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Whitlock, K. E. "Development of Drosophila wing sensory neurons in mutants with missing or modified cell surface molecules." Development 117, no. 4 (April 1, 1993): 1251–60. http://dx.doi.org/10.1242/dev.117.4.1251.

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The neurons of the sensory receptors on the wing of Drosophila melanogaster have highly characteristic axon projections in the central nervous system (CNS). The morphology of these projections was studied in flies bearing mutations that affect cell surface molecules thought to be important in axon guidance. The animals used were mutant for the fasciclinI (fasI), fasciclinII (fasII), fasciclinIII (fasIII) and neurally altered carbohydrate (nac) genes. Axon populations were visualized by staining with DiI and light-reacting the dye with diaminobenzidine to yield permanent preparations. The fasI, fasII and fasIII mutants as well as the nac mutant display altered axonal trajectories in the CNS. One phenotype seen in fasII mutants and in animals mutant for both fasI and fasIII was extra branching within the axon projection pattern. A second phenotype observed was a reduction or complete loss of one of the tracts, apparently due to the axons shifting to a neighboring tract. This was seen in the most extreme form in nac mutants and to a lesser degree in fasIII mutants. To determine if the mutations discussed here affected axon guidance, wing discs were analyzed using the antibody 22C10 to label sensory neurons in the wing during metamorphosis. Both misrouting of axons and the appearance of ectopic neurons in the wing were observed. In the fasI:fasIII, the fasII and the nac mutants, there was misrouting of sensory axons in the developing wing. In addition, the fasII and nac mutants displayed ectopic sensory neurons in the wing. This implies that the cell surface molecules missing (fasciclins) or modified (by the nac gene product), in these mutants may play a role in both neurogenesis and axon guidance.
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Hao, Hailing, and David I. Shreiber. "Axon Kinematics Change During Growth and Development." Journal of Biomechanical Engineering 129, no. 4 (February 14, 2007): 511–22. http://dx.doi.org/10.1115/1.2746372.

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The microkinematic response of axons to mechanical stretch was examined in the developing chick embryo spinal cord during a period of rapid growth and myelination. Spinal cords were isolated at different days of embryonic (E) development post-fertilization (E12, E14, E16, and E18) and stretched 0%, 5%, 10%, 15%, and 20%, respectively. During this period, the spinal cord grew ∼55% in length, and white matter tracts were myelinated significantly. The spinal cords were fixed with paraformaldehyde at the stretched length, sectioned, stained immunohistochemically for neurofilament proteins, and imaged with epifluorescence microscopy. Axons in unstretched spinal cords were undulated, or tortuous, to varying degrees, and appeared to straighten with stretch. The degree of tortuosity (ratio of the segment’s pathlength to its end-to-end length) was quantified in each spinal cord by tracing several hundred randomly selected axons. The change in tortuosity distributions with stretch indicated that axons switched from non-affine, uncoupled behavior at low stretch levels to affine, coupled behavior at high stretch levels, which was consistent with previous reports of axon behavior in the adult guinea pig optic nerve (Bain, Shreiber, and Meaney, J. Biomech. Eng., 125(6), pp. 798–804). A mathematical model previously proposed by Bain et al. was applied to quantify the transition in kinematic behavior. The results indicated that significant percentages of axons demonstrated purely non-affine behavior at each stage, but that this percentage decreased from 64% at E12 to 30% at E18. The decrease correlated negatively to increases in both length and myelination with development, but the change in axon kinematics could not be explained by stretch applied during physical growth of the spinal cord. The relationship between tissue-level and axonal-level deformation changes with development, which can have important implications in the response to physiological forces experienced during growth and trauma.
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Dissertations / Theses on the topic "Axon development"

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Wyatt, Cameron. "Optic axon guidance during development and regeneration in the zebrafish." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5947.

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Directed regeneration of axons in the CNS has potential for the treatment of CNS disorders and injuries. In contrast to mammals, following optic nerve lesion zebrafish regenerate axons that navigate to their correct targets and form new synapses leading to functional recovery. Correct pathfinding is thought to rely on a range of molecular cues in the CNS which the growing axon expresses receptors for. However, the specific guidance cues are not well elucidated. It is likely that a proportion of them will be the same as during development, while some may be specific to regeneration. Alternatively, axons may simply retrace former trajectories guided by the molecular environment or mechanical constraints of degenerating tracts, as demonstrated in the mammalian PNS. To elucidate this, we investigated regeneration in the astray/robo2 knockout mutant which exhibits misprojection of optic axons during development leading to the establishment of ectopic tracts. We show that degenerating tracts do not provide a strong guidance cue for regenerating axons in the CNS as ectopic tracts in the astray mutant are not repopulated following lesion despite presenting a similar environment to entopic degenerating tracts. We also find that as astray mutant (knockout) and robo2 morphant (transient knockdown) projection and termination errors persist in the adult, it is clear that there is not an efficient correction mechanism for large-scale pathfinding errors of optic axons during development. In addition, we find a reduced importance of the axon guidance receptor Robo2 and its repellent ligand Slit2 for pathfinding during regeneration as specific developmental pathfinding errors of optic axons in astray mutants are corrected during adult optic nerve regeneration and global overexpression of Slit2 elicits pathfinding defects during development but not regeneration. To address regeneration-associated gene regulation in axotomised retinal ganglion cells, we carried out a microarray analysis. We found that many genes detected as a gradient in the adult retina during regeneration are not differentially expressed in the embryonic eye, despite having distinct expression patterns in other embryonic tissues. Of the genes which exhibit strong differential expression in the retina of both regenerating adults and developing embryos, foxI1 is one of the most interesting candidates as other fox genes have been implicated in axon guidance and due to its highly restricted retinal expression pattern. Surprisingly, further investigation has revealed that foxI1 knockout mutant embryos have retinotectal projections which appear normal in terms of axon pathfinding and mapping. Another family of genes indicated by the array, which are cytosolic phosphoproteins known to be involved in the signal transduction cascade of multiple inhibitory guidance cues during axon growth, are the crmps. Knocking down crmp2 with morpholinos during development resulted in a sparser innervation of the tectum with individual axons which trend towards having less complex arbors with shorter branches and reduced overall axon length. As a whole this work adds to our current knowledge of optic axon guidance during development and regeneration and the relative importance and effect of selected potential guidance cues, which may help toward informing future mammalian CNS regeneration research.
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Lickiss, Thomas. "Development of directed initial axon outgrowth in the cerebral neocortex." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543013.

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Yeomans, Heather Jane. "Investigations into the functions of immunoglobulin like cell adhesion molecules during vertebrate neural development." Thesis, University of Sheffield, 2001. http://etheses.whiterose.ac.uk/5986/.

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During neural development, each neuron sends an axon out from its cell body. Extending axons are guided by interactions between environmental factors and axonal receptors for these factors. It has been suggested that certain proteins of the immunoglobulin-like superfamily are among the molecules involved in axon guidance. In particular, TAG-1, Ll and NrCAM have previously been implicated in the guidance of dorsal spinal commissural axons at the ventral midline region known as the floor plate. To establish whether these molecules have such roles in mice, the dorsal spinal axons of TAG-1, L1 or NrCAM mutant mouse embryos were traced. There were no significant differences between the results from mutant embryos and their wild type counterparts. This indicated that these three proteins are individually not essential for the normal development of mouse dorsal spinal projections. However, results from TAG-MLI double mutant embryos suggested that TAG- I and LI might affect the ability of commissural axons to extend out of the floor plate. Analysis of ephrin B3 mutant embryos indicated that ephrin B3 might also be important for floor plate exit. As the TAG-1 null mutation includes a lacZ construct, this reporter gene was used to further investigate the roles of TAG-1. Its expression was used to determine distribution of TAG-1 gene activity in the developing mouse nervous system. As the pattern of reporter expression was found to be comparable with that of TAG-1 protein, the TAG-1 null allele was used as a marker for TAG-1-expressing cells in mutant embryos. Most of the structures that normally express TAG-1 seemed to be unaffected by an absence of the protein. However, the hypoglossal nerve was significantly less likely to extend towards the tongue in TAG-1 null homozygous embryos than in heterozygotes. This suggested that TAG-1 might be important for the guidance of hypoglossal axons.
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Ibrahim, Merdol. "Axon-oligodendrocyte relations in the anterior medullary velum of the rat brain." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263729.

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Kamkar, Fatemeh. "Pftaire1 (Cyclin Dependent Kinase14): Role and Function in Axonal Outgrowth During the development of the CNS." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32860.

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Cyclin Dependent Kinase (Cdk) family members play a role in CNS development. Cyclin Dependent Kinase 5 (Cdk5) is well known for its fundamental role in neuronal development and axogenesis, as well as, cell death. Other Cdks include Pctaire and Pftaire. Inhibition of Pctaire results in increased axon outgrowth, however, the role and function of Pftaire is unknown. Pftaire1 is a novel member of the Cdk family that was initially detected in a screen for cdc2-like kinases. Unpublished data from our lab reveals that Pftaire1 (Eip63E) deficiency in Drosophila melanogaster results in defects in the axon and neuronal structure of the ventral nerve cord (VNC). In mammals, Pftaire1 is highly, expressed in the CNS. Here, we proposed that Pftaire1 might have a role in axon outgrowth. To investigate the role of Pftaire1 in mammals, the first germline Pftaire1 knockout mice were generated. Considering the severe effects of Eip63E deficiency in Drosophila and the homology between mammalian and fly Pftaire1, CNS defects in the mouse were anticipated. However, to date, no gross abnormalities have been detected in the overall morphology, fertility, life span, or anatomical brain structures of the Pftaire1 deficient mice. This may be due to the presence of other post-mitotic Cdk proteins that are highly similar to Pftaire1. For instance, mammals possess Pftaire (1, and 2), as well as, Pctaire (1, 2, and 3), while Drosophila only possess the Pftaire1 orthologue where the Pftaire2 and Pctaire (1, 2, and 3) are absent. Furthermore, the mice were of mixed background. In spite of this, we demonstrated that Pftaire1 deficient neurons showed increased axon length, in the initial phases of culture. This was confirmed by expression of dominant negative (DN) D228N-Pftaire1 in wild type neurons. Also classification of axons into different ranges, reveals a higher percentage of hyperextended neurites in D228N and Pftaire1 knockout mice. The mechanism by which Pftaire1 controls axon outgrowth is unknown. In this study we show that, Pftaire1 interacts physically with the small GTPase proteins Rac1, Cdc42, and RhoA. Importantly, we showed that Pftaire1 phosphorylates GDP-RhoA on a serine residue. We propose that this regulates RhoA activity, which in turn controls axon outgrowth.
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Zhang, Ye. "The role of the secretory pathway in dendrite and axon development." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3390087.

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Wang, Xinshuo Snider William D. "Glycogen synthase kinase-3 is required for axon growth and development." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2435.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Sep. 3, 2009). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Cell and Molecular Physiology in School of Medicine." Discipline: Cell and Molecular Physiology; Department/School: Medicine.
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Steinel, Martin C. "Flamingo/Starry night in embryonic abdominal sensory axon development of Drosophila /." Connect to thesis, 2008. http://repository.unimelb.edu.au/10187/3144.

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Huberman, Andrew David. "Neural activity and axon guidance cue regulation of eye-specific retinogeniculate development /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2004. http://uclibs.org/PID/11984.

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Clegg, James Matthew. "Role of transcription factor Pax6 in the development of the thalamocortical tract." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8099.

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During development the nuclei of the thalamus form reciprocal connections with specific regions within the cortex. These connections give rise to the thalamocortical tract. The processes by which axons of the thalamocortical tract are guided to their target regions are poorly understood. It has been shown that diffusible or membrane bound factors can have a chemoattractive or chemorepulsive effect on the tip or growth cone of the axon. Thalamocortical axons may also be guided along ‘pioneer’ axon populations that form a scaffold along which axons may grow. The transcription factor Pax6 has been shown to have a role in a variety of developmental processes such as neuronal patterning, proliferation, migration and axon guidance. It is known that Pax6 is involved in the development of the thalamocortical tract but its exact role is unknown. To explore the role that Pax6 plays in the development of the thalamocortical tract I have used two different mouse models, the small eye (Pax6Sey/Sey) mouse which lacks functional Pax6, and a conditional Pax6 knock-out (Pax6cKO) mouse made using a Gsh2 Cre line that specifically reduces Pax6 expression in the ventral telencephalon and prethalamus. Using the Pax6Sey/Sey mouse I show that thalamocortical axons do not enter the ventral telencephalon in the absence of Pax6 and that a small number of axons incorrectly enter the hypothalamus. In addition axons found within the ventral telencephalon of the mutant do not originate from the thalamus but instead originate from cells within the ventral telencephalon itself. I have found that the expression of guidance molecule Robo2 is reduced in the Pax6Sey/Sey mouse, which may explain why thalamocortical axons enter the hypothalamus. When Pax6 expression is reduced at the prethalamus and ventral telencephalon using the Pax6cKO mouse I show that the majority of thalamocortical axons reach the cortex normally but some axons become disorganized within the thalamus. Pioneer axons which emanate from the prethalamus normally guide thalamocortical axons through the diencephalon but in the Pax6cKO I report that these axons are reduced which may explain the disorganization of thalamocortical axons within the thalamus. Taken together the data from these two models demonstrate that for the thalamocortical tract to form normally Pax6 expression is required in both the cells of the thalamus and in cells that lie along the route of the tract. In addition I provide evidence that Pax6 may influence axon guidance by controlling the expression of guidance molecules and the development of pioneer axon tracts.
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Books on the topic "Axon development"

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Zoltán, Molnár. Development of thalamocortical connections. Berlin: Springer, 1998.

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Bagnard, Dominique, and Various. Axon Growth and Guidance. Springer, 2010.

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Dominique, Bagnard, ed. Axon growth and guidance. New York: Springer Science + Business Media, 2007.

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Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.
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Trakhtenberg, Ephraim F., and Jeffrey Louis Goldberg. Axon Growth and Regeneration. Elsevier Science & Technology Books, 2012.

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Trakhtenberg, Ephraim F., and Jeffrey Louis Goldberg. Axon Growth and Regeneration. Elsevier Science & Technology Books, 2012.

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Hajime, Fujisawa, ed. Molecular basis of axon growth and nerve pattern formation. Tokyo: Japan Scientific Societies Press, 1997.

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Borah, Joylaxmi Saikia. Action research for alternative development: A study of women agricultural and subsistence workers in Axom. 1999.

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Kostovic, Ivica. Guidance Cues in the Developing Brain (Progress in Molecular and Subcellular Biology). Springer, 2003.

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Turner, Martin R., Matthew C. Kiernan, and Kevin Talbot. Technical advances in neuroscience. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0001.

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This chapter highlights key technological advances in neuroimaging, the understanding of impulse transmission, and the molecular biology of the nervous system that have underpinned our modern understanding of the brain, mind, and nervous system. Neuroimaging spans the sub-cellular and systems levels of neuroscience, beginning with electron microscopy and then, 50 years later, magnetic resonance imaging and increasingly sophisticated mathematical modelling of brain function. These developments have been interleaved with the improved understanding of neurotransmission, starting with the seminal observations made from giant squid axon recordings, which were translated into clinically useable tools through the application of electric current, and later with magnetic stimulation. It is during the last 50 years that a molecular framework for these concepts emerged, with the cloning of genes that began in Duchenne muscular dystrophy, paving the way for the wider human genome project.
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Book chapters on the topic "Axon development"

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McLellan, Tracey. "Axon." In Encyclopedia of Child Behavior and Development, 194–95. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_268.

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Yamashita, Masayuki. "Retinal Strip Culture for Studying Ganglion Cell Axon Growth." In Retinal Development, 55–64. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0175-4_5.

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Masu, Masayuki. "Emerging Roles of Heparan Sulfate in Axon Guidance Signaling." In Cortical Development, 203–14. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54496-8_9.

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Yamamoto, Nobuhiko, Takuro Maruyama, Naofumi Uesaka, Yasufumi Hayano, Makoto Takemoto, and Akito Yamada. "Molecular Mechanisms of Thalamocortical Axon Targeting." In Cortical Development: Genes and Genetic Abnormalities, 199–211. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470994030.ch14.

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Ohno, Nobuhiko, Takashi Sakoh, Yurika Saitoh, Nobuo Terada, and Shinichi Ohno. "Schwann Cell–Axon Interactions: The Molecular and Metabolic Link Between Schwann Cells and Axons." In Schwann Cell Development and Pathology, 47–67. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54764-8_4.

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Lemmon, Vance, Kathryn Farr, and Carl Lagenaur. "Neuronal Surface Receptors in Axon Fasciculation and Regeneration." In Cell Interactions in Visual Development, 113–31. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3920-8_7.

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Luck, Robert, and Carmen Ruiz de Almodovar. "Axon Guidance Factors in Developmental and Pathological Angiogenesis." In Endothelial Signaling in Development and Disease, 259–91. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2907-8_11.

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Berry, M., S. M. Hall, E. L. Rees, P. Yiu, and J. Sievers. "The Role of Basal Lamina in Axon Regeneration." In Mesenchymal-Epithelial Interactions in Neural Development, 361–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-71837-3_28.

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Tytell, Michael. "Characterization of Glial Proteins Transferred into the Squid Giant Axon." In Glial-Neuronal Communication in Development and Regeneration, 247–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71381-1_16.

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Piper, Michael, Amber-Lee S. Dawson, Charlotta Lindwall, Guy Barry, Céline Plachez, and Linda J. Richards. "Emx and Nfi Genes Regulate Cortical Development and Axon Guidance in the Telencephalon." In Cortical Development: Genes and Genetic Abnormalities, 230–45. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470994030.ch16.

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Conference papers on the topic "Axon development"

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Qi Xu, Fang Chen, Yuanyuan Wang, Xiao Li, and Jiping He. "Development of a miniaturized bioreactor for neural culture and axon stretch growth." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6943865.

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Akizawa, Y., Y. Morita, Y. Hsu, T. Yamaoka, and E. Nakamachi. "Development of IKVAV Modified PLLA Guide Tube Having Unidirectional Fibers on Inner Surface to Enhance Axonal Extension." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66458.

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The bi-layer poly-L-lactic acid (PLLA) guide tube for peripheral nerve regeneration was developed by electrospinning method to enhance axonal extension. The inner layer of the guide tube had unidirectional nanofiber and Ile-Lys-Val-Ala-Val (IKVAV) modified surface. IKVAV modified unidirectional fiber sheets which had different fiber diameters from 400 to 1200 nm were fabricated to optimize fiber diameter of the guide tube for axonal extension. Fiber sheets without the IKVAV were prepared as the control group. PC12 cells seeded on the fiber sheets were cultured for 6 days. Axons were most extended in fiber diameter of 1090 nm with IKVAV and 1160 nm without IKVAV. Maximum axon length increased by about 25% due to IKVAV modification. The bi-layer guide tube which had fiber diameter about 1133 nm was fabricated. It was confirmed that the inner layer had unidirectional fibers and the outer layer had random fibers in the guide tube. CS, which corresponds to radial compressive stiffness, of the guide tube and the sciatic nerve were 230 N/mm2 and 1.64 N/mm2 respectively. Since radial compressive stiffness of the guide tube was higher than that of the sciatic nerve, the developed guide tube was expected to enhance axonal extension without narrowing.
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Kulathu, Sandeep, and David L. Littlefield. "Development of a Biofidelic Material Model for Brain Tissue." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53136.

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Computational simulations of brain injury mechanisms have advanced to a level of sophistication where in addition to capturing different anatomic regions, the computational mesh is capable of distinguishing white and grey matter in the brain. Brain tissue is typically modeled as an isotropic, viscoelastic material. Experiments have shown that the mechanical response of brain tissue to an external load varies depending on the location from which the tissue is harvested and also the direction of loading. Some researchers have developed anisotropic constitutive models by appealing to the composite material case wherein cylindrical axon fibers are immersed in a cellular matrix. Though such material models have been developed over a small sample, they have not been applied over the entire brain for simulation purposes.
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Sundararaghavan, Harini G., Gary A. Monteiro, and David I. Shreiber. "Guided Axon Growth by Gradients of Adhesion in Collagen Gels." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-69124.

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During development, neurites are directed by gradients of attractive and repulsive soluble (chemotactic) cues and substrate-bound adhesive (haptotactic) cues. Many of these cues have been extensively researched in vitro, and incorporated into strategies for nerve and spinal cord regeneration, primarily to improve the regenerative environment. To enhance and direct growth, we have developed a system to create 1D gradients of adhesion through a 3D collagen gel using microfluidics. We test our system using collagen grafted with bioactive peptide sequences, IKVAV and YIGSR, from laminin — an extra-cellular matrix (ECM) protein known to strongly influence neurite outgrowth. Gradients are established from ∼0.37mg peptide/mg collagen – 0, and ∼0.18 mg peptide/mg collagen – 0 of each peptide and tested using chick dorsal root ganglia (DRG). Neurite growth is evaluated 5 days after gradient formation. Neurites show increased growth in the gradient system when compared to control and biased growth up the gradient of peptides. Growth in YIGSR-grafted collagen increased with steeper gradients, whereas growth in IKVAV-grafted collagen decreased with steeper gradients. These results demonstrate that neurite growth can be enhanced and directed by controlled, immobilized, haptotactic gradients through 3D scaffolds, and suggest that including these gradients in regenerative therapies may accelerate nerve and spinal cord regeneration.
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Elias, Ragi A. I., Jason Maikos, and David I. Shreiber. "Mechanical Properties of the Chick Embryo Spinal Cord." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176773.

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Determining the mechanical properties of the spinal cord are useful to identify its response to sub-injurious loading experienced during normal motion, to evaluate the biomechanics of spinal cord injury (SCI) [1], and to understand the role of the changing mechanical environment in growth and development. While an array of studies have focused on the mechanical properties of adult spinal cords, those properties may not be the same as pediatric spinal cords, which undergoes significant changes during development. Additionally, during embryonic and fetal development, axon growth and neural precursor differentiation into neurons are at their peak.
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Sotudeh-Chafi, M., N. Abolfathi, A. Nick, V. Dirisala, G. Karami, and M. Ziejewski. "A Multi-Scale Finite Element Model for Shock Wave-Induced Axonal Brain Injury." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192342.

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Traumatic brain injuries (TBIs) involve a significant portion of human injuries resulting from a wide range of civilian accidents as well as many military scenarios. Axonal damage is one of the most common and important pathologic features of traumatic brain injury. Axons become brittle when exposed to rapid deformations associated with brain trauma. Accordingly, rapid stretch of axons can damage the axonal cytoskeleton, resulting in a loss of elasticity and impairment of axoplasmic transport. Subsequent swelling of the axon occurs in discrete bulb formations or in elongated varicosities that accumulate organelles. Ultimately, swollen axons may become disconnected [1]. The shock waves generated by a blast, subject all the organs in the head to displacement, shearing and tearing forces. The brain is especially vulnerable to these forces — the fronts of compressed air waves cause rapid forward or backward movements of the head, so that the brain rattles against the inside of the skull. This can cause subdural hemorrhage and contusions. The forces exerted on the brain by shock waves are known to damage axons in the affected areas. This axonal damage begins within minutes of injury, and can continue for hours or days following the injury [2]. Shock waves are also known to damage the brain at the subcellular level, but exactly how remains unclear. Kato et al., [3] described the effects of a small controlled explosion on rats’ brain tissue. They found that high pressure shock waves led to contusions and hemorrhage in both cortical and subcortical brain regions. Based on their result, the threshold for shock wave-induced brain injury is speculated to be under 1 MPa. This is the first report to demonstrate the pressure-dependent effect of shock wave on the histological characteristics of brain tissue. An important step in understanding the primary blast injury mechanism due to explosion is to translate the global head loads to the loading conditions, and consequently damage, of the cells at the local level and to project cell level and tissue level injury criteria towards the level of the head. In order to reach this aim, we have developed a multi-scale non-linear finite element modeling to bridge the micro- and macroscopic scales and establish the connection between microstructure and effective behavior of brain tissue to develop acceptable injury threshold. Part of this effort has been focused on measuring the shock waves created from a blast, and studying the response of the brain model of a human head exposed to such an environment. The Arbitrary Lagrangian Eulerian (ALE) and Fluid/Solid Interactions (FSI) formulation have been used to model the brain-blast interactions. Another part has gone into developing a validated fiber-matrix based micro-scale model of a brain tissue to reproduce the effective response and to capturing local details of the tissue’s deformations causing axonal injury. The micro-model of the axon and matrix is characterized by a transversely isotropic viscoelastic material and the material model is formulated for numerical implementation. Model parameters are fit to experimental frequency response of the storage and loss modulus data obtained and determined using a genetic algorithm (GA) optimizing method. The results from macro-scale model are used in the micro-scale brain tissue to study the effective behavior of this tissue under injury-based loadings. The research involves the development of a tool providing a better understanding of the mechanical behavior of the brain tissue against blast loads and a rational multi-scale approach for driving injury criteria.
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Murakami, S., Y. Morita, and E. Nakamachi. "Development of Bio-MEMS Device for Cell Cluster Patterning by Using Dielectrophoresis Method." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64295.

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Recently, the investigation of cell-activation and tissue regeneration process has shown the great progress in the biomedical and biomechanical research fields. In this study fabricated Biomedical-Micro Electric Mechanical System (Bio-MEMS) to examine accurately the cell activation by introducing the cell patterning assignment technique, which consists of the photolithograph method to generate the MEMS device and the cell patterning technique by using the dielectrophoresis (DEP) method. In the development of Bio-MEMS devices for cell culture and micro-bioreactor system, unresolved subjects, 1) the fundamental mechanism of cell activation, 2) the flow control of culture medium 3) the accurate cell pattern technique and 4) the implementation of positive DEP methods, are remained. In this study, we fabricate 2-D patterns of point by using the DEP method introducing the positive effects and the trap method by employing the gravity effect and the adhesion technique, to reveal the fundamental mechanism of cell activations, such as the nerve cell axon extension. We succeed to establish the cell patterning technique by using a novel electrode design technique, such as 2-D patterns of point. The results is shown that our novel approach using comprehensive designed electrodes is superior to cell patterning. Therefore, our device able to produce neural network consists of a large number of cells.
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Uchaikin, Sergey, Yoshiro Urade, Shingo Kono, Matthias Schmelz, Ronny Stolz, Yasunobu Nakamura, Andrei Matlashov, et al. "Development of SQUID Amplifiers for Axion Search Experiments." In 2019 IEEE International Superconductive Electronics Conference (ISEC). IEEE, 2019. http://dx.doi.org/10.1109/isec46533.2019.8990953.

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Nakagawa, K., T. Takaki, Y. Morita, and E. Nakamachi. "2D Phase-Field Analyses of Axonal Extension of Nerve Cell." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64281.

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In this study, we aimed to develop a computer-aided simulation technique to predict the axonal extension in the neuronal network evolution processes for design new scaffolds to activate the nerve cell and promote the nerve regeneration. We developed a mathematical model of axonal extension by using phase-field method and evaluated the validity of the mathematical model by comparison with the experiments. In the previous experimental studies, the peripheral nerve scaffold has been introduced to guide the axonal extension. Damaged part of nerve was replaced by the artificial tube as the scaffold to induce the axonal growth through the artificial tube and regenerate the nerve network. However, the scaffold made of biodegradable materials has a problem that it is degraded and absorbed before the nerve regenerate, and then the nerve cannot regenerate. Therefore, there is a need for the design and development of a scaffold for nerve regeneration to promote nerve regeneration. For that purpose, it is necessary to understand the difference between the axonal extensions by the surrounding environment, such as the shape or materials of the scaffold for nerve regeneration. In particular, the numerical technique to analyze the remodeling process of the nerve in the scaffold is strongly required to be established because the in-vivo experimental observation technology at the micro scale, bioethical issues in the animal experiment and requires time and money are also remained as unresolved problems. In this study, we developed a new simulation code which employed the phase-field method to predict the two-dimensional dendritic and axonal growth processes of nerve cells on cultivation scaffolds. We curried out the phase-field analyses to make clear how the parameters of Kobayashi–Warren–Carter (KWC) phase-field model affected on the morphologic growths of dendrite and axon. Simultaneously, we had observed the axonal extension process by using the PC-12D cells with nerve growth factor (NGF) on two-dimensional cultivation dish. Based on these axonal extension observation results, we approximated the morphological changes and establish the phenomenological model for phase-field analysis. Finally, we confirmed the validity of our newly developed phase-field simulation scheme in two dimensions by comparison with the experiments.
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Sigal, Ian A., Hongli Yang, Michael D. Roberts, Claude F. Burgoyne, and J. Crawford Downs. "Biomechanics of the Posterior Pole During the Remodeling Progression From Normal to Early Experimental Glaucoma." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206518.

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Glaucoma is one of the leading causes of blindness worldwide. The loss of vision associated with glaucoma is due to damage to the retinal ganglion cell axons, which transmit visual information to the brain. Damage to these axons is believed to occur as the axons pass through the lamina cribrosa (LC), a connective tissue structure in the optic nerve head at the back of the eye. Elevated intraocular pressure (IOP) has been identified as the main risk factor for the development of the neuropathy, but the mechanism(s) by which a mechanical insult (elevated IOP) is translated into a biological effect (glaucomatous optic neuropathy) is not well understood.
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Reports on the topic "Axon development"

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Selleck, Scott B. Understanding the Function of Tuberous Sclerosis Complex Genes in Neural Development: Roles in Synapse Assembly and Axon Guidance. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada603854.

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Kim, Young Jin. Development of New Directions in Axion Dark Matter Searches. Office of Scientific and Technical Information (OSTI), March 2019. http://dx.doi.org/10.2172/1501785.

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