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Relevant bibliographies by topics / Embryonic chick spinal cord

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Academic literature on the topic 'Embryonic chick spinal cord'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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Journal articles on the topic "Embryonic chick spinal cord"

1

Stewart, Gregory R., John W. Olney, Maya Pathikonda, and William D. Snider. "Excitotoxicity in the embryonic chick spinal cord." Annals of Neurology 30, no. 6 (December 1991): 758–66. http://dx.doi.org/10.1002/ana.410300604.

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Ono, K., R. Bansal, J. Payne, U. Rutishauser, and R. H. Miller. "Early development and dispersal of oligodendrocyte precursors in the embryonic chick spinal cord." Development 121, no. 6 (June 1, 1995): 1743–54. http://dx.doi.org/10.1242/dev.121.6.1743.

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Oligodendrocytes, the myelinating cells of the vertebrate CNS, originally develop from cells of the neuroepithelium. Recent studies suggest that spinal cord oligodendrocyte precursors are initially localized in the region of the ventral ventricular zone and subsequently disperse throughout the spinal cord. The characteristics of these early oligodendrocyte precursors and their subsequent migration has been difficult to assay directly in the rodent spinal cord due to a lack of appropriate reagents. In the developing chick spinal cord, we show that oligodendrocyte precursors can be specifically identified by labeling with O4 monoclonal antibody. In contrast to rodent oligodendrocyte precursors, which express O4 immunoreactivity only during the later stages of maturation, in the chick O4 immunoreactivity appears very early and its expression is retained through cellular maturation. In embryos older than stage 35, O4+ cells represent the most immature, self-renewing, cells of the chick spinal cord oligodendrocyte lineage. In the intact chick spinal cord, the earliest O4+ cells are located at the ventral ventricular zone where they actually contribute to the ventricular lining of the central canal. The subsequent migration of O4+ cells into the dorsal region of the spinal cord temporally correlates with the capacity of isolated dorsal spinal cord to generate oligodendrocytes in vitro. Biochemical analysis suggests O4 labels a POA-like antigen on the surface of chick spinal cord oligodendrocyte precursors. These studies provide direct evidence for the ventral ventricular origin of spinal cord oligodendrocytes, and suggest that this focal source of oligodendrocytes is a general characteristic of vertebrate development.

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Hasan, Sohail J., Brad H. Nelson, J. Ignacio Valenzuela, Hans S. Keirstead, Sarah E. Shull, Douglas W. Ethell, and John D. Steeves. "Functional repair of transected spinal cord in embryonic chick." Restorative Neurology and Neuroscience 2, no. 3 (1991): 137–54. http://dx.doi.org/10.3233/rnn-1991-2303.

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Weill, Cheryl L. "Characterization of androgen receptors in embryonic chick spinal cord." Developmental Brain Research 24, no. 1-2 (January 1986): 127–32. http://dx.doi.org/10.1016/0165-3806(86)90180-x.

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Sholomenko, G. N., and M. J. O'Donovan. "Development and characterization of pathways descending to the spinal cord in the embryonic chick." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 1223–33. http://dx.doi.org/10.1152/jn.1995.73.3.1223.

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1. We used an isolated preparation of the embryonic chick brain stem and spinal cord to examine the origin, trajectory, and effects of descending supraspinal pathways on lumbosacral motor activity. The in vitro preparation remained viable for < or 24 h and was sufficiently stable for electrophysiological, pharmacological, and neuroanatomic examination. In this preparation, as in the isolated spinal cord, spontaneous episodes of both forelimb and hindlimb motor activity occur in the absence of phasic afferent input. Motor activity can also be evoked by brain stem electrical stimulation or modulated by the introduction of neurochemicals to the independently perfused brain stem. 2. At embryonic day (E)6, lumbosacral motor activity could be evoked by brain stem electrical stimulation. At E5, neither brain stem nor spinal cord stimulation evoked activity in the lumbosacral spinal cord, although motoneurons did express spontaneous activity. 3. Lesion and electrophysiological studies indicated that axons traveling in the ventral cord mediated the activation of lumbosacral networks by brain stem stimulation. 4. Partition of the preparation into three separately perfused baths, using a zero-Ca2+ middle bath that encompassed the cervical spinal cord, demonstrated that the brain stem activation of spinal networks could be mediated by long-axoned pathways connecting the brain stem and lumbosacral spinal cord. 5. Using retrograde tracing from the spinal cord combined with brain stem stimulation, we found that the brain stem regions from which spinal activity could be evoked lie in the embryonic reticular formation close to neurons that send long descending axons to the lumbosacral spinal cord. The cells giving rise to these descending pathways are found in the ventral pontine and medullary reticular formation, a region that is the source of reticulospinal neurons important for motor activity in adult vertebrates. 6. Electrical recordings from this region revealed that the activity of some brain stem neurons was synchronized with the electrical activity of lumbosacral motoneurons during evoked or spontaneous episodes of rhythmic motor activity. 7. Both brain stem and spinal cord activity could be modulated by selective application of the glutamate agonist N-methyl-D-aspartate to the brain stem, supporting the existence of functionally active descending projections from the brain stem to the spinal cord. It is not yet clear what role the brain stem activity carried by these pathways has in the genesis and development of spinal cord motor activity.

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Chilton, John K., and Andrew W. Stoker. "Expression of Receptor Protein Tyrosine Phosphatases in Embryonic Chick Spinal Cord." Molecular and Cellular Neuroscience 16, no. 4 (October 2000): 470–80. http://dx.doi.org/10.1006/mcne.2000.0887.

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Vogel, M. W. "Activation patterns of embryonic chick lumbosacral motoneurones following large spinal cord reversals." Journal of Physiology 389, no. 1 (August 1, 1987): 491–512. http://dx.doi.org/10.1113/jphysiol.1987.sp016668.

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8

Weill, C. L. "Somatostatin (SRIF) Prevents Natural Motoneuron Cell Death in Embryonic Chick Spinal Cord." Developmental Neuroscience 13, no. 6 (1991): 377–81. http://dx.doi.org/10.1159/000112188.

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9

Leber, SM, and JR Sanes. "Migratory paths of neurons and glia in the embryonic chick spinal cord." Journal of Neuroscience 15, no. 2 (February 1, 1995): 1236–48. http://dx.doi.org/10.1523/jneurosci.15-02-01236.1995.

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10

Arai, Yoshiyasu, Yoko Momose-Sato, Katsushige Sato, and Kohtaro Kamino. "Optical Mapping of Neural Network Activity in Chick Spinal Cord at an Intermediate Stage of Embryonic Development." Journal of Neurophysiology 81, no. 4 (April 1, 1999): 1889–902. http://dx.doi.org/10.1152/jn.1999.81.4.1889.

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Optical mapping of neural network activity in chick spinal cord at an intermediate stage of embryonic development. We have applied multiple-site optical recording of transmembrane potential changes to recording of neuronal pathway/network activity from embryonic chick spinal cord slice preparations. Spinal cord preparations were dissected from 8-day-old chick embryos at Hamburger-Hamilton stage 33, and transverse slice preparations were prepared with the 13th cervical spinal nerve or with the 2nd or 5th lumbosacral spinal nerve intact. The slice preparations were stained with a voltage-sensitive merocyanine-rhodanine dye (NK2761). Transmembrane voltage-related optical (dye-absorbance) changes evoked by spinal nerve stimulation with positive square-current pulses using a suction electrode were recorded simultaneously from many loci in the preparation, using a 128- or 1,020-element photodiode array. Optical responses were detected from dorsal and ventral regions corresponding to the posterior (dorsal) and anterior (ventral) gray horns. The optical signals were composed of two components, fast spike-like and slow signals. In the dorsal region, the fast spike-like signal was identified as the presynaptic action potential in the sensory nerve and the slow signal as the postsynaptic potential. In the ventral region, the fast spike-like signal reflects the antidromic action potential in motoneurons, and the slow signal is related to the postsynaptic potential evoked in the motoneuron. In preparations in which the ventral root was cut microsurgically, the antidromic action potential-related optical signals were eliminated. The areas of the maximal amplitude of the evoked signals in the dorsal and ventral regions were located near the dorsal root entry zone and the ventral root outlet zone, respectively. Quasiconcentric contour-line maps were obtained in the dorsal and ventral regions, suggesting the functional arrangement of the dorsal and ventral synaptic connections. Synaptic fatigue induced by repetitive stimuli in the ventral synapses was more rapid than in the dorsal synapses. The distribution patterns of the signals were essentially similar among C13, LS2, and LS5 preparations, suggesting that there is no difference in the spatiotemporal pattern of the neural responses along the rostrocaudal axis of the spinal cord at this developmental stage. In the ventral root-cut preparations, comparing the delay times between the ventral slow optical signals, we have been able to demonstrate that neural network-related synaptic connections are generated functionally in the embryonic spinal cord at Hamburger-Hamilton stage 33.

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Dissertations / Theses on the topic "Embryonic chick spinal cord"

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Chilton, John K. "The role of receptor protein tyrosine phosphatases in axon guidance." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365814.

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Hanson, Martin Gartz Jr. "THE EMBRYONIC NEURAL CIRCUIT: MECHANISM AND INFLUENCE OF SPONTANEOUS RHYTHMIC ACTIVITY IN EARLY SPINAL CORD DEVELOPMENT." Case Western Reserve University School of Graduate Studies / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=case1085515804.

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Baillie-Johnson, Peter. "The generation of a candidate axial precursor in three dimensional aggregates of mouse embryonic stem cells." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267818.

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Textbook accounts of vertebrate embryonic development have been based largely upon experiments on amphibian embryos, which have shown that the tissues of the trunk and tail are organised from distinct precursors that existed during gastrulation. In the mouse and chick, however, retrospective clonal analyses and transplantation experiments have demonstrated that the amniote body instead arises progressively from a population of axial precursors that are common to both the neural and mesodermal tissues of the trunk and tail. For this reason, they are known as neuro-mesodermal progenitors (NMps). Detailed studies of NMps have been precluded by their lack of a unique gene expression profile and the technical difficulties associated with isolating them from the embryo. Mouse embryonic stem cells (ESCs) provide the possibility of instead deriving them in vitro. ESCs have been used to model developmental processes, partly through large cellular aggregates known as embryoid bodies. These structures do not, however, resemble the axial organisation of the embryo and they develop in a disordered manner. This thesis presents a novel culture system of small, three-dimensional aggregates of ESCs (gastruloids) that can recreate the events of early post-implantation development, including axial elongation. Gastruloids are the first ESC-based model for axial elongation morphogenesis; this body of work characterises their development and identifies a candidate population of NMps within their elongating tissues. Additionally, this work establishes a xenotransplantation assay for testing the functional properties of in vitro-derived NMp populations in the chicken embryo and applies it to NMps from gastruloid cultures. The results of this assay show that gastruloids are a credible source of NMps in vitro and therefore offer a new experimental means to interrogate their properties. The use of gastruloids to recreate embryonic development has implications for basic research as a synthetic system and for the therapeutic derivation of other embryonic progenitors through bioengineering.

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Ethell, Douglas Wayne. "Analysis of developing chick Gallus domesticus spinal cord proteins using two dimensional gel electrophoresis." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29834.

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Several recent experiments on developing chick spinal cord have established a time window when the developing spinal cord changes from a permissive to a restrictive environment for regeneration. This time window occurs during embryonic days 13-14 (E13-E14) of chick development. Recent experiments in adult rat, have found two proteins that actively inhibit axonal regeneration. This study has sought possible inhibitory proteins, in chicks, correlating to this temporal change. Proteins continuously present after this change (E14-E20) but not before (E11) were identified. Two-dimensional gel electrophoresis was used for separatation of the proteins. Seven protein spots of interest demonstrated this correlative late-expressing neural protein (LNP) profile. Although the functions of these proteins could not be ascertained in this study, further investigation is warranted.
Science, Faculty of
Zoology, Department of
Graduate

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Lim, Tit Meng. "Segmentation in the nervous system of the chick embryo." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329053.

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Rigato, Chiara. "Role of microglial cells during the mouse embryonic spinal cord development." Paris 6, 2013. http://www.theses.fr/2013PA066326.

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Le but de mon projet de thèse a été d’investiguer le rôle des cellules microgliales in vivo au cours du développement. On s’est particulièrement intéressés au développement de la moelle épinière car ce modèle a été bien caractérisé. Nous avons trouvé que les microglies colonisent la moelle épinière embryonnaire grâce à leur migration et prolifération. A E12. 5 les microglies s’accumulent transitoirement au point d’insertion des ganglions de la racine dorsale et phagocytent les axons apoptotiques des neurones sensoriels. A E13. 5 les microglies interagissent avec les glies radiaires, expriment la galactin-3 et phagocytent les corps apoptotiques de motoneurones (Rigato et al. , 2011). Ces microglies sont capables de proliférer grâce au récepteur P2X7 qui n’est pas couplé à l’hémicanal pannexin-1. Ce récepteur ne contrôle pas l’activation, ce qui indique que pendant le développement embryonnaire de la moelle épinière, la prolifération et l’activation microgliale sont deux processus indépendants (Rigato et al. , 2012). Actuellement nous sommes en train d’analyser le rôle des microglies dans l’apoptose en utilisant des embryons PU. 1-KO, génétiquement dépourvus de microglies. En l’absence de microglies, le nombre de motoneurones et neurones sensoriels qui rentrent en apoptose augmente. Les cellules microgliales semblent donc avoir un rôle protecteur vis à vis de motoneurones, probablement à travers la sécrétion de facteurs de croissance. Ces résultats montrent que les interactions microglies-neurones sont établies très tôt au cours du développement de la moelle épinière et ils ouvrent un nouveau champ de recherche qui permettra de mieux comprendre comment se forment ces interactions
The challenge of my PhD project has been to understand more about embryonic microglial cells in vivo in the developing CNS. I focus my attention to the developing mouse spinal cord as it is a deeply studied and well-characterized model. We found that microglial cells colonize the embryonic spinal cord through migration and proliferation. At E12. 5 microglia transitory accumulate at the insertion point of dorsal root ganglia (DRG) and phagocytose apoptotic axons of sensory neurons. At E13. 5 microglia interact with radial glial cells, express the galactin-3 and phagocytose the apoptotic bodies of dying motoneurons (Rigato et al. , 2001). These ventral microglia at E13. 5 are able to proliferate as they express the purinergic receptor P2X7 that are not coupled to pannexin-1 hemichannel. This receptor strictly controls microglial proliferation but it is not involved in their activation, indicating that during the embryonic development of the spinal cord, microglial proliferation and activation are two independent processes (Rigato et al. , 2012). We are now analysing the putative role of microglia in the developmental cell death process by using PU. 1-KO embryos, genetically devoid of microglial cells. In absence of microglia, the number of motoneurons and sensory neurons that undergo programmed cell death increased. Microglial cells seem to have a protective role towards neurons, probably through the release of some growth factors. These results show that that interactions between microglia and neurons are established very early during spinal cord development and they open a new research field that will permit to better understand how these interactions are formed

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Schaeffer, Julia. "The molecular regulation of spinal nerve outgrowth." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271632.

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During amniote embryogenesis, the segmented pattern characteristic of the vertebral column appears early during development through the sequential formation of multipotent structures called somites. Somites differentiate subsequently into dermomyotome (giving rise later to skin and skeletal muscles) and sclerotome (giving rise to vertebral bone structures and cartilage). In addition, sclerotomes subdivide following their rostro-caudal intrasegmental boundary into an axon growth-permissive region (anterior half) and an axon growth-repulsive region (posterior half). This binary system instructs motor and sensory axon navigation, as well as neural crest cell migration, to ensure that the peripheral nervous system develops without obstruction by the future cartilage and bones of the vertebral column. Repellent cues are expressed in posterior half-sclerotomes in order to exclude navigating axons from “no-go” areas and restrict their growth to specific exit points of the future vertebral column. Interestingly, similar repellent cues (e.g. Eph/Ephrins) are expressed in the adult central nervous system (CNS) and have been shown to control connectivity and plasticity throughout life. Following brain or spinal cord injury, these repellent molecules are upregulated by reactive astrocytes accumulating at the lesion site, and may impede axon regeneration in this region. In this dissertation, I am presenting the results of a differential gene expression analysis of anterior and posterior half-sclerotomes, based on RNA-sequencing data and using the chick embryo as a model organism. This study led to the identification of molecules, previously uncharacterized in this system, that may play a role in adhesive and mechanical properties of somites and in axon guidance and fasciculation. I focused on the functional analysis of one molecule of the posterior half-sclerotome, the extracellular matrix protein Fibulin-2. To look at its role in the segmentation of spinal axons, I used ectopic misexpression in a subset of segments based on somite electroporation. The width of spinal nerve bundle growth was restricted by Fibulin-2 overexpression in posterior and anterior half-sclerotomes, suggesting a role in sharpening/controlling the path of spinal axon growth. In addition, I showed that this could occur via an interaction with the axon growth repellent Semaphorin 3A. Then I looked at the expression of Fibulin-2 in two models of CNS injury: mouse cerebral cortical stab injury and rat dorsal crush spinal cord injury. In both cases, I observed an increase in Fibulin-2 protein level compared to control. I also used primary cultures of rat cortical astrocytes to show that the expression of Fibulin-2 after inflammatory cytokine-induced activation is increased. Finally, I studied a candidate axon growth repellent previously identified in the laboratory. I explored the hypothesis that this repellent molecule is an O-glycosylated, spliced variant form of a known protein. To characterize this repellent molecule, I used RNA-sequencing data from chick embryonic somites and 2D gel electrophoresis of an astrocytic cell line protein extract. Together, these results suggested that the developing vertebral column and the adult CNS share molecular features to control axon growth and plasticity. This type of study could lead to the characterization of molecular systems that regulate axon growth, and to the identification of novel therapeutic targets in brain or spinal cord injury.

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Withers, Michelle Dawn. "Regulation of glycine receptors by embryonic rat spinal cord neurons during development in vitro." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187369.

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This work addresses developmental regulation of neurotransmitter receptors in the vertebrate central nervous system (CNS). Glycine receptors (GlyR) play a major role in inhibitory neurotransmission in the spinal cord. Changes in the types of GlyRs being expressed by embryonic rat spinal cord neurons are examined during development in vitro. Spinal cord neurons are cultured at the fourteenth day of gestation, prior to receiving afferent input. Previous work demonstrated a delayed expression of the adult-type GlyR α subunits. Reverse transcriptase-polymerase chain reaction demonstrates the presence of mRNA for GlyR α2 subunits by these neurons at early times in culture. The presence of GlyR α2 subunits are confirmed by immunofluorescence microscopy with a new α2 subunit specific antibody. These subunits appear by the first day in culture and exhibit a diffuse subcellular distribution. During the course of these experiments, populations of embryonic rats were found to differ in the subtypes of GlyR they expressed at early times during development. The expression of functional GlyRs is investigated in two populations of embryonic rats using whole-cell patch clamp recordings. The GlyR antagonist, strychnine, is used as a tool to distinguish between some forms of the GlyR. The two populations are similar in their onset of responsiveness to glycine and in the ion-dependence of the glycine-induced current. The strychnine-sensitivity of responses to glycine differs between the two populations. Neurons from the first population of rats exhibit a developmentally regulated increase in the sensitivity to strychnine, while the strychnine-sensitivity of responses to glycine by neurons from the second population remains high throughout development in culture. These results suggest that two populations differ in the type of functional GlyR they express during early development in culture. The relatively low sensitivity to strychnine exhibited during the first few days in culture by neurons from the first population of rats cannot be accounted for by changes in sensitivity to glycine or by non-specific cross-activation of γ-aminobutyric acid receptors (GABARs). Neurons from the first population undergo a gradual change from the predominant expression of a strychnine-insensitive GlyR to some form(s) of strychnine-sensitive GlyR.

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Swinnen, Nina. "Microglia in the embryonic brain and spinal cord during the development of neuronal networks." Paris 6, 2013. http://www.theses.fr/2013PA066321.

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Les cellules microgliales sont les cellules immunitaires résidentes du système nerveux central (SNC). Elles peuvent déjà être détectées au début du développement embryonnaire du SNC. Dans ce projet de recherche nous avons étudié l'invasion et les caractéristiques phénotypiques des cellules microgliales du cerveau embryonnaire. Nos résultats demontrent que les microglies dans le cortex embryonnaire ont un phénotype de « repos »; elles expriment peu de marqueurs d'activation et n'ont presque aucun canaux K+ à rectification entrante. Pourtant, elles sont très dynamiques comme dans le cerveau adulte. Au cours du développement du plexus choroïde, des microglies activées au phenotype phagocytique s'accumulent à un moment coïncidant avec un pic d'apoptose dans cette structure. La proliferation des microglies dans la moelle épinière embryonnaire dépend de récepteurs P2X7. Nous avons retrouvé les mêmes récepteurs sur les cellules microgliales du cortex. Diverses études ont demontré que les infections et l'activation immunitaire pendant la grossesse donnent un risque accru de développement de maladies neuro-psychiatriques chez les enfants. Puisque les microglies sont les cellules immunitaires du SNC et qu’elles sont présentes au cours du développement embryonnaire, nous avons examiné si elles sont activées après une reaction immunitaire maternelle pendant la grossesse. Nos résultats indiquent qu’il n'y a aucune augmentation de densité ou d’activation des cellules microgliales dans le cerveau embryonnaire après induction d’une réaction immunitaire maternelle
The microglia are the resident immune cells of the central nervous system (CNS). They can be detected from the beginning of the development of the embryonic CNS. In this project we have studied the invasion and phenotypic characteristics of the microglial cells in the embryonic brain. Our results show that embryonic microglia in the cortex have a “resting” phenotype; the express little activation markers and have little to no inward rectifying K+ channels. However, they are very dynamic like observed in the adult brain. During development of the choroid plexus, activated microglia with a phagocytic phenotype accumulate at the moment apoptotic cells are present in this structure. The proliferation of microglial in the embryonic spinal cord depends on P2X7 receptors. We found the same receptors to be present on the microglia in the cortex. Different studies have shown that infections and immune activation during pregnancy increase the risk on neuropsychiatric disorders in the offspring. Since microglia are the immune cells of the CNS and they are present early in development, we studied the effect of maternal inflammation during pregnancy on these cells. Our results indicate that there is no effect on microglia density and activation after maternal immune activation

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Che, Mohamad Che Anuar. "Human embryonic stem cell-derived mesenchymal stem cells as a therapy for spinal cord injury." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/7047/.

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Traumatic injury to the spinal cord interrupts ascending and descending pathways leading to severe functional deficits of sensory motor and autonomic function which depend on the level and severity of the injury. There are currently no effective therapies for treating such injuries and the adult central nervous system has very limited capacity for repair so that recovery is very limited and functional deficits are usually permanent. Cell transplantation is a potential therapy for spinal cord injury and a range of cell types are being investigated as candidates. Mesenchymal stem cells (MSCs) obtained from bone marrow are one cell type quite extensively studied. When transplanted into animal models of spinal cord injury these cells are reported to affect various aspects of repair and in some cases to improve functional outcome according to behavioural measures. However, the use of these cells has several limitations including the need for an invasive harvesting procedure, variability in cell quality and slow expansion in culture. This project therefore had two main aims: Firstly to investigate whether MSC-like cells closely equivalent to bone marrow derived MSCs could be reliably and consistently differentiated from human embryonic stem cells (hESCs) in order to provide an “off the shelf” cellular therapy product for spinal cord injury and secondly, to transplant such cells into animal models of spinal cord injury in order to, determine whether hESC-derived MSCs replicate or improve on the repair mechanisms reported for bone marrow MSCs.

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Books on the topic "Embryonic chick spinal cord"

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Inevitable collision: The inspiring story that brought stem cell research to conservative America. Rochelle, NY: Mary Ann Liebert, Inc., Publishers, 2015.

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McLaughlin, Hooley Michael Graham. Morphological patterning and stability in the regenerating spinal cord of the chick embryo. 1985.

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Mason, Peggy. Developmental Overview of Central Neuroanatomy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0003.

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The central nervous system develops from a proliferating tube of cells and retains a tubular organization in the adult spinal cord and brain, including the forebrain. Failure of the neural tube to close at the front is lethal, whereas failure to close the tube at the back end produces spina bifida, a serious neural tube defect. Swellings in the neural tube develop into the hindbrain, midbrain, diencephalon, and telencephalon. The diencephalon sends an outpouching out of the cranium to form the retina, providing an accessible window onto the brain. The dorsal telencephalon forms the cerebral cortex, which in humans is enormously expanded by growth in every direction. Running through the embryonic neural tube is an internal lumen that becomes the cerebrospinal fluid–containing ventricular system. The effects of damage to the spinal cord and forebrain are compared with respect to impact on self and potential for improvement.

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Book chapters on the topic "Embryonic chick spinal cord"

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Tabak, Joel, Peter Wenner, and Michael J. O’Donovan. "Rhythm Generation in Embryonic Chick Spinal Cord." In Encyclopedia of Computational Neuroscience, 1–6. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7320-6_45-2.

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Tabak, Joel, Peter Wenner, and Michael J. O’Donovan. "Rhythm Generation in Embryonic Chick Spinal Cord." In Encyclopedia of Computational Neuroscience, 1–6. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_45-3.

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Tabak, Joel, Peter Wenner, and Michael J. O’Donovan. "Rhythm Generation in Embryonic Chick Spinal Cord." In Encyclopedia of Computational Neuroscience, 2642–47. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_45.

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Wang, Hui, and Michael P. Matise. "In Ovo Electroporation in Embryonic Chick Spinal Cords." In Methods in Molecular Biology, 133–40. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-444-9_13.

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O’Donovan, M., and A. Ritter. "Rhythmic Activity Patterns of Motoneurones and Interneurones in the Embryonic Chick Spinal Cord." In Neural Control of Movement, 195–201. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1985-0_25.

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Wichterle, Hynek, Mirza Peljto, and Stephane Nedelec. "Xenotransplantation of Embryonic Stem Cell-Derived Motor Neurons into the Developing Chick Spinal Cord." In Methods in Molecular Biology, 171–83. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-060-7_11.

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Mayer-Pröschel, Margot. "Cell differentiation in the embryonic mammalian spinal cord." In Advances in Research on Neurodegeneration, 1–8. Vienna: Springer Vienna, 1999. http://dx.doi.org/10.1007/978-3-7091-6369-6_1.

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Noronha, M. J. "Embryonic Development of the Spinal Cord and Associated Disorders." In Clinical Medicine and the Nervous System, 79–93. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3353-7_7.

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Reier, Paul J., John Q. Trojanowski, Virginia M.-Y. Lee, and Margaret J. Velardo. "Studies of a Human Neuron-Like Cell Line in Stroke and Spinal Cord Injury." In Human Embryonic Stem Cells, 345–87. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-423-8_18.

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O’Donovan, Michael J., and Amy Ritter. "Optical Recording and Lesioning of Spinal Neurones During Rhythmic Activity in the Chick Embryo Spinal Cord." In Alpha and Gamma Motor Systems, 557–63. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1935-5_122.

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Conference papers on the topic "Embryonic chick spinal cord"

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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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Shreiber, David I., Hailing Hao, and Ragi A. I. Elias. "The Effects of Glia on the Tensile Properties of the Spinal Cord." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190184.

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Glia, the primary non-neuronal cells of the central nervous system, were initially believed to bind or glue neurons together and/or provide a supporting scaffold [1, 2]. It is now recognized that these cells provide specialized and essential biological and regulatory functions. Still, their contributions to the overall mechanical properties would also strongly influence the tissue’s tolerance to loading conditions experienced during trauma and potentially regulate of function and growth in neurons and glia [3, 4]. White matter represents an intriguing tissue to appreciate the role of glia in tissue and cellular mechanics. White matter consists of bundles of axons aligned in parallel, which are myelinated by oligodendrocytes, and a network of astrocytes, which interconnect axons and the vascular supply. In this study, we selectively interfered with the glial network during chick embryo development and evaluated the tensile properties of the spinal cord. Myelination was suppressed by injecting ethidium bromide (EB), which is cytotoxic to dividing cells and kills oligodendrocytes and astrocytes, or an antibody against galactocerebroside (αGalC) with serum complement, which interferes with oligodendrocytes during the myelination process without affecting astrocytes.

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Fournier, Adam, Suneil Hosmane, and K. T. Ramesh. "Thresholds for Embryonic CNS Axon Integrity, Degeneration, and Regrowth Using a Focal Compression Platform." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80331.

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Traumatic axonal injuries (TAI) are broadly defined as the focal or multi-focal damage of axons within white matter tracts of the central nervous system (CNS), and can occur in the setting of spinal cord injury (SCI) and traumatic brain injury (TBI). TAI can result from mechanical forces associated with the rapid deformation of white matter regions during trauma. Through combinations of compression, stretch, and shear, axon injury often results in an irreversible loss of functional neural connectivity, since the scope for axonal regeneration in the CNS is extremely limited.

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Sundararaghavan, Harini G., Gary A. Monteiro, and David I. Shreiber. "Microfluidic Generation of Adhesion Gradients Through 3D Collagen Gels: Implications for Neural Tissue Engineering." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192987.

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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 [1, 2]. Gradients are established from 0.14 mg/ml–0, and 0.07 mg/ml–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. 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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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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Sundararaghavan, Harini G., and David I. Shreiber. "Gradients of Stiffness Guide Neurite Growth in 3D Collagen Gels." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41873.

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One approach to enhance nerve and spinal cord regeneration following injury is to implant a biomaterial scaffold to ”bridge” the gap of the injury. Structural/mechanical anisotropy has been suggested as a means of orienting this growth axially. We have spatially varied the mechanical properties of a 3D collagen gel to direct growth axially and unidirectionally. Gradients of mechanical properties were generated in collagen gels by exposing the collagen to a 0–1mM gradient of genipin, a cell-tolerated crosslinking agent, for 12hrs via microfluidics. The gradient of stiffness was confirmed via a gradient of genipin-induced fluorescence intensity, which we have previously correlated to the storage modulus of collagen gels. The growth of neurites from isolated chick embryo dorsal root ganglia (DRG) in the presence of these gradients was evaluated after 5 days in culture. In control cases, neurites grew into the collagen gel and up either side of the cross-channel to approximately equal lengths. A 20% difference in differential growth was observed in control experiments. In contrast, when presented a gradient of shear modulus from ∼365Pa – 60Pa, neurites elected to grow down the gradient of stiffness to the compliant side, with an almost 300% difference. Interestingly, the length of neurites in gels with gradients was significantly greater than the length of those grown in gels with uniform, untreated gels with high compliance. Control of neurite growth, cell migration, and other aspects of cell behavior in 3D scaffolds via mechanical properties offers vast potential for tissue engineering and other regenerative therapies.

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