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Journal articles on the topic 'Embryonic chick spinal cord'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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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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2

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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3

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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4

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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5

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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6

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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7

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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11

Arai, Yoshiyasu, Yoko Momose-Sato, Katsushige Sato, and Kohtaro Kamino. "337 Optical monitoring of neural responses in the embryonic chick spinal cord slice." Neuroscience Research 28 (January 1997): S65. http://dx.doi.org/10.1016/s0168-0102(97)90168-1.

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12

Antal, Miklós, and Erika Polgár. "Development of Calbindin-D28k Immunoreactive Neurons in the Embryonic Chick Lumbosacral Spinal Cord." European Journal of Neuroscience 5, no. 7 (July 1993): 782–94. http://dx.doi.org/10.1111/j.1460-9568.1993.tb00930.x.

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13

Fedirchuk, Brent, Peter Wenner, Patrick J. Whelan, Stephen Ho, Joel Tabak, and Michael J. O’Donovan. "Spontaneous Network Activity Transiently Depresses Synaptic Transmission in the Embryonic Chick Spinal Cord." Journal of Neuroscience 19, no. 6 (March 15, 1999): 2102–12. http://dx.doi.org/10.1523/jneurosci.19-06-02102.1999.

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14

Gotoh, Hitoshi, Katsuhiko Ono, Hirohide Takebayashi, Harukazu Nakamura, Hidekiyo Harada, and Kazuhiro Ikenaka. "Generation of somatic motoneurons from Nkx2.2-expressing progenitor cells in chick embryonic spinal cord." Neuroscience Research 71 (September 2011): e344. http://dx.doi.org/10.1016/j.neures.2011.07.1509.

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15

Weill, Cheryl L. "Characterization of glucocorticoid receptors in whole and cellular subfractions of embryonic chick spinal cord." Developmental Brain Research 27, no. 1 (June 1986): 167–73. http://dx.doi.org/10.1016/0165-3806(86)90242-7.

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16

Joshi, Piyush, and Isaac Skromne. "A theoretical model of neural maturation in the developing chick spinal cord." PLOS ONE 15, no. 12 (December 18, 2020): e0244219. http://dx.doi.org/10.1371/journal.pone.0244219.

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Cellular differentiation is a tightly regulated process under the control of intricate signaling and transcription factors interaction network working in coordination. These interactions make the systems dynamic, robust and stable but also difficult to dissect. In the spinal cord, recent work has shown that a network of FGF, WNT and Retinoic Acid (RA) signaling factors regulate neural maturation by directing the activity of a transcription factor network that contains CDX at its core. Here we have used partial and ordinary (Hill) differential equation based models to understand the spatiotemporal dynamics of the FGF/WNT/RA and the CDX/transcription factor networks, alone and in combination. We show that in both networks, the strength of interaction among network partners impacts the dynamics, behavior and output of the system. In the signaling network, interaction strength determine the position and size of discrete regions of cell differentiation and small changes in the strength of the interactions among networking partners can result in a signal overriding, balancing or oscillating with another signal. We also show that the spatiotemporal information generated by the signaling network can be conveyed to the CDX/transcription network to produces a transition zone that separates regions of high cell potency from regions of cell differentiation, in agreement with most in vivo observations. Importantly, one emerging property of the networks is their robustness to extrinsic disturbances, which allows the system to retain or canalize NP cells in developmental trajectories. This analysis provides a model for the interaction conditions underlying spinal cord cell maturation during embryonic axial elongation.

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17

Crittenden, S. L., R. S. Pratt, J. H. Cook, J. Balsamo, and J. Lilien. "Immunologically unique and common domains within a family of proteins related to the retina Ca2+-dependent cell adhesion molecule, NcalCAM." Development 101, no. 4 (December 1, 1987): 729–40. http://dx.doi.org/10.1242/dev.101.4.729.

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Rabbit polyclonal antibodies raised to gp90, a fragment of the embryonic chick neural retina Ca2+-dependent adhesive molecule, gp130, recognize gp130 and inhibit Ca2+-dependent cell-cell adhesion. When tested against a panel of 10-day embryonic tissues, one of these antisera recognizes a component with a molecular weight identical to that of gp130 in embryonic chick cerebrum, optic lobe, hind brain, spinal cord and neural retina only; the second antiserum recognizes a similar component in all of the embryonic chick tissues tested. These data imply the existence of an extended family of closely related cell surface components with immunologically distinct subgroups each of which may mediate Ca2+-dependent cell-cell adhesion. As the term CAM, or cell adhesion molecule, has become common usage we propose to refer to these molecules as calCAMs, reflecting their calcium dependence. Analysis of fragments and endoglycosidase digests of NcalCAM have allowed a comparison of its structure with similar molecules from different tissues and species that have been implicated in Ca2+-dependent cell-cell adhesion.

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18

Matise, M. P., and C. Lance-Jones. "A critical period for the specification of motor pools in the chick lumbosacral spinal cord." Development 122, no. 2 (February 1, 1996): 659–69. http://dx.doi.org/10.1242/dev.122.2.659.

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When 3–4 segments of the chick lumbosacral neural tube are reversed in the anterior-posterior axis at stage 15 (embryonic day 2.5), the spinal cord develops with a reversed organization of motoneurons projecting to individual muscles in the limb (C. Lance-Jones and L. Landmesser (1980) J. Physiol. 302, 581–602). This finding indicated that motoneuron precursors or components of their local environment were specified with respect to target by stage 15. To identify the timing of this event, we have now assessed motoneuron projections after equivalent neural tube reversals at earlier stages of development. Lumbosacral neural tube segments 1–3 (+/− one segment cranial or caudal) were reversed in the anterior-posterior axis at stages 13 and 14 (embryonic day 2). The locations of motoneurons innervating two thigh muscles, the sartorius and femorotibialis, were mapped via retrograde horseradish peroxidase labeling at stages 35–36 (embryonic days 9–10). In a sample of embryos, counts were made of the total number of motoneurons in the lateral motor columns of reversed segments. The majority of motoneurons projecting to the sartorius and femorotibialis were in a normal position within the spinal cord. Segmental differences in motor column size were also similar to normal. These observations indicate that positional cues external to the LS neural tube can affect motoneuron commitment and number at stages 13–14. Since these observations stand in contrast to results following stage 15 reversals, we conclude that regional differences related to motoneuron target identity are normally specified or stabilized within the anterior LS neural tube between stages 14 and 15. To examine the role of the notochord in this process, neural tube reversals were performed at stages 13–14 as described above, except that the underlying notochord was also reversed. Projections to the sartorius and femorotibialis muscles did not differ significantly from those in embryos with neural tube reversals alone, indicating that the notochord is not the source of cues for target identity at stages 13–14.

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19

Wenner, Peter, Michael J. O'Donovan, and Michael P. Matise. "Topographical and Physiological Characterization of Interneurons That Express Engrailed-1 in the Embryonic Chick Spinal Cord." Journal of Neurophysiology 84, no. 5 (November 1, 2000): 2651–57. http://dx.doi.org/10.1152/jn.2000.84.5.2651.

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A number of homeodomain transcription factors have been implicated in controlling the differentiation of various types of neurons including spinal motoneurons. Some of these proteins are also expressed in spinal interneurons, but their function is unknown. Progress in understanding the role of transcription factors in interneuronal development has been slow because the synaptic connections of interneurons, which in part define their identity, are difficult to establish. Using whole cell recording in the isolated spinal cord of chick embryos, we assessed the synaptic connections of lumbosacral interneurons expressing the Engrailed-1 (En1) transcription factor. Specifically we established whether En1-expressing interneurons made direct connections with motoneurons and whether they constitute a single interneuron class. Cells were labeled with biocytin and subsequently processed for En1 immunoreactivity. Our findings indicate that the connections of En1-expressing cells with motoneurons and with sensory afferents were diverse, suggesting that the population was heterogeneous. In addition, the synaptic connections we tested were similar in interneurons that expressed the En1 protein and in many that did not. The majority of sampled En1 cells did, however, exhibit a direct synaptic connection to motoneurons that is likely to be GABAergic. Because our physiological methods underestimate the number of direct connections with motoneurons, it is possible that the great majority, perhaps all, En1-expressing cells make direct synaptic connections with motoneurons. Our results raise the possibility that En1 could be involved in interneuron-motoneuron connectivity but that its expression is not restricted to a distinct functional subclass of ventral interneuron. These findings constrain hypotheses about the role of En-1 in interneuron development and function.

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20

Mochida, Hiraku, Katsushige Sato, Yoshiyasu Arai, Shinichi Sasaki, Itaru Yazawa, Kohtaro Kamino, and Yoko Momose-Sato. "Multiple-site optical recording reveals embryonic organization of synaptic networks in the chick spinal cord." European Journal of Neuroscience 13, no. 8 (April 2001): 1547–58. http://dx.doi.org/10.1046/j.0953-816x.2001.01528.x.

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21

Linares, A., G. J. Caama�o, R. Diaz, F. J. Gonzalez, and E. Garcia-Peregrin. "Utilization of ketone bodies by chick brain and spinal cord during embryonic and postnatal development." Neurochemical Research 18, no. 10 (October 1993): 1107–12. http://dx.doi.org/10.1007/bf00966692.

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22

Ritter, Amy, Peter Wenner, Stephen Ho, Patrick J. Whelan, and Michael J. O’Donovan. "Activity Patterns and Synaptic Organization of Ventrally Located Interneurons in the Embryonic Chick Spinal Cord." Journal of Neuroscience 19, no. 9 (May 1, 1999): 3457–71. http://dx.doi.org/10.1523/jneurosci.19-09-03457.1999.

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23

Murphy, AE, H. Peek, ML Baudet, and S. Harvey. "Extrapituitary GH in the chicken: underestimation of immunohistochemical staining by Carnoy's fixation." Journal of Endocrinology 177, no. 2 (May 1, 2003): 223–34. http://dx.doi.org/10.1677/joe.0.1770223.

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GH has previously been shown to be present in peripheral extrapituitary tIssues of chick embryos, but the cellular distribution of GH immunoreactivity is still uncertain because of differing immunohistochemical findings. The possibility that this uncertainty reflects differences in fixation of the embryonic tIssues was assessed by comparing GH immunoreactivity in tIssues fixed in 4% (w/v) paraformaldehyde or Carnoy's fluid (60% ethanol (v/v); 30% chloroform (v/v); 10% acetic acid (v/v)). A widespread distribution of GH immunoreactivity was seen in paraformaldehyde-fixed tIssues, although it was particularly intense in the spinal cord, dorsal and ventral root ganglia, notochord, myotome, epidermis, crop, heart, lung and humerus. In marked contrast, GH immunoreactivity in embryonic tIssues fixed with Carnoy's was more discrete and mainly restricted to marginal and mantle layers of the spinal cord, spinal nerves, the ventral root ganglia and the extensor nerve of the anterior limb bud. Since these are neural derivatives, Carnoy's fixation appears to preferentially result in neural GH staining, whereas GH staining in neural and non-neural tIssues is seen after paraformaldehyde fixation. Carnoy's, because it is a precipitive fixative, may only fix large GH moieties, whereas GH in peripheral tIssues includes numerous molecular variants, many of which are of relatively small size. Paraformaldehyde, because it is a cross-linking fixative, preferentially fixes peptides and small proteins, and it may therefore fix more GH moieties than Carnoy's fluid. Carnoy's fixation appears to underestimate GH immunoreactivity in immunohistochemical studies on the cellular distribution of GH-like proteins in embryonic chicks.

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24

Grady, M. S., O. Steward, and J. A. Jane. "Transplantaion of embryonic chick spinal cord into transection adult chicken into transection adult chicken spinal cords: A useful model for transplantation research." Journal of Neuroscience Research 14, no. 4 (1985): 403–14. http://dx.doi.org/10.1002/jnr.490140403.

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25

Momose-Sato, Yoko, Katsushige Sato, and Kohtaro Kamino. "Unusual optical signal related to depolarization spreading over the embryonic chick spinal cord-brainstem-cerebrum preparation." Neuroscience Research 31 (January 1998): S114. http://dx.doi.org/10.1016/s0168-0102(98)81974-3.

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26

Arai, Yoshiyasu, Yoko Momose-Sato, Katsushige Sato, and Kohtaro Kamino. "Optical demonstration of the functional formation of neural circuits in the embryonic chick spinal cord slice." Neuroscience Research 31 (January 1998): S115. http://dx.doi.org/10.1016/s0168-0102(98)81975-5.

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27

Carr, Patrick A., and Peter Wenner. "Calcitonin gene-related peptide: distribution and effects on spontaneous rhythmic activity in embryonic chick spinal cord." Developmental Brain Research 106, no. 1-2 (March 1998): 47–55. http://dx.doi.org/10.1016/s0165-3806(97)00191-0.

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28

Bradley, Douglas M., Francesca D. Beaman, D. Blaine Moore, Kara Kidd, and Marieta Barrow Heaton. "Neurotrophic factors BDNF and GDNF protect embryonic chick spinal cord motoneurons from ethanol neurotoxicity in vivo." Developmental Brain Research 112, no. 1 (January 1999): 99–106. http://dx.doi.org/10.1016/s0165-3806(98)00155-2.

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29

Lyles, Joan Martin, and Cheryl L. Weill. "Changes in Glucose 6-Phosphate Dehydrogenase Activity in Developing Embryonic Chick Skeletal Muscle and Spinal Cord." Developmental Neuroscience 8, no. 1 (1986): 44–52. http://dx.doi.org/10.1159/000112240.

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30

Park, Sang Wook, Ha Seong Lim, Eun Jung Roh, Dong Woon Kim, Gye Sun Jeon, and Sa Sun Cho. "Developmental Expression of Transferrin Binding Protein in Oligodendrocyte Lineage Cells of the Embryonic Chick Spinal Cord." Neurochemical Research 32, no. 1 (December 6, 2006): 11–18. http://dx.doi.org/10.1007/s11064-006-9216-6.

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31

Dow, Kimberly E., Douglas W. Ethell, John D. Steeves, and Richard J. Riopelle. "Molecular Correlates of Spinal Cord Repair in the Embryonic Chick: Heparan Sulfate and Chondroitin Sulfate Proteoglycans." Experimental Neurology 128, no. 2 (August 1994): 233–38. http://dx.doi.org/10.1006/exnr.1994.1132.

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32

Yang, J., and C. F. Zorumski. "Trifluoperazine blocks GABA-gated chloride currents in cultured chick spinal cord neurons." Journal of Neurophysiology 61, no. 2 (February 1, 1989): 363–73. http://dx.doi.org/10.1152/jn.1989.61.2.363.

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1. The effects of trifluoperazine (TFP) on gamma-aminobutyric acid- (GABA) gated chloride currents were investigated using cultured chick embryonic spinal cord neurons (SCN) and gigaseal patch clamp recording techniques. 2. TFP showed a dose-dependent attenuation of GABA responses with half-maximal block near 9 microM. The GABA antagonism was noncompetitive and voltage dependent with greater block at hyperpolarized potentials. 3. At 10 microM, GABA induced little desensitization in response to prolonged applications in the absence of TFP. At 100 microM, GABA responses desensitized with a time constant near 27 s. Coapplication of TFP did not alter the lack of desensitization to 10 microM GABA but revealed a second, faster component (time constant approximately 0.7 s) to the attenuation at 100 microM GABA. 4. Steady-state fluctuation analysis of the macroscopic GABA-gated current gave a power spectrum that was described by a simple Lorentzian function. The corner frequency of fluctuations to GABA [34.6 +/- 7.3 (SE) Hz] remained unchanged during simultaneous application of GABA and TFP (33.0 +/- 8.5 Hz), indicating that TFP does not alter the average GABA channel open duration. 5. Single-channel recording from isolated outside-out membrane patches showed GABA-gated chloride events with a primary conductance of 26 pS and a minor component (representing less than 5% of all events) of 10 pS. With simultaneous application of GABA and TFP, event amplitudes remained unchanged but the frequency of opening was decreased. 6. The distribution of the main conductance channel open times were well described by the sum of two exponentials with time constants of 0.82 +/- 0.18 and 7.4 +/- 2.0 ms. These time constants were not significantly altered by 50 microM TFP. 7. TFP, at 100 microM, attenuated responses to (% of control): GABA (7.5 +/- 2.3), glycine (15.4 +/- 5.5), and glutamate (64.5 +/- 5.5). The proconvulsant tendency of TFP, in part, may be due to the greater block of responses to inhibitory than to excitatory transmitters.

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33

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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34

Wenner, Peter, and Michael J. O'Donovan. "Mechanisms That Initiate Spontaneous Network Activity in the Developing Chick Spinal Cord." Journal of Neurophysiology 86, no. 3 (September 1, 2001): 1481–98. http://dx.doi.org/10.1152/jn.2001.86.3.1481.

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Many developing networks exhibit a transient period of spontaneous activity that is believed to be important developmentally. Here we investigate the initiation of spontaneous episodes of rhythmic activity in the embryonic chick spinal cord. These episodes recur regularly and are separated by quiescent intervals of many minutes. We examined the role of motoneurons and their intraspinal synaptic targets (R-interneurons) in the initiation of these episodes. During the latter part of the inter-episode interval, we recorded spontaneous, transient ventral root depolarizations that were accompanied by small, spatially diffuse fluorescent signals from interneurons retrogradely labeled with a calcium-sensitive dye. A transient often could be resolved at episode onset and was accompanied by an intense pre-episode (∼500 ms) motoneuronal discharge (particularly in adductor and sartorius) but not by interneuronal discharge monitored from the ventrolateral funiculus (VLF). An important role for this pre-episode motoneuron discharge was suggested by the finding that electrical stimulation of motor axons, sufficient to activate R-interneurons, could trigger episodes prematurely. This effect was mediated through activation of R-interneurons because it was prevented by pharmacological blockade of either the cholinergic motoneuronal inputs to R-interneurons or the GABAergic outputs from R-interneurons to other interneurons. Whole-cell recording from R-interneurons and imaging of calcium dye-labeled interneurons established that R-interneuron cell bodies were located dorsomedial to the lateral motor column (R-interneuron region). This region became active before other labeled interneurons when an episode was triggered by motor axon stimulation. At the beginning of a spontaneous episode, whole-cell recordings revealed that R-interneurons fired a high-frequency burst of spikes and optical recordings demonstrated that the R-interneuron region became active before other labeled interneurons. In the presence of cholinergic blockade, however, episode initiation slowed and the inter-episode interval lengthened. In addition, optical activity recorded from the R-interneuron region no longer led that of other labeled interneurons. Instead the initial activity occurred bilaterally in the region medial to the motor column and encompassing the central canal. These findings are consistent with the hypothesis that transient depolarizations and firing in motoneurons, originating from random fluctuations of interneuronal synaptic activity, activate R-interneurons, which then trigger the recruitment of the rest of the spinal interneuronal network. This unusual function for R-interneurons is likely to arise because the output of these interneurons is functionally excitatory during development.

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Haimson, Baruch, Oren Meir, Reut Sudakevitz-Merzbach, Gerard Elberg, Samantha Friedrich, Peter V. Lovell, Sónia Paixão, Rüdiger Klein, Claudio V. Mello, and Avihu Klar. "Natural loss of function of ephrin-B3 shapes spinal flight circuitry in birds." Science Advances 7, no. 24 (June 2021): eabg5968. http://dx.doi.org/10.1126/sciadv.abg5968.

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Flight in birds evolved through patterning of the wings from forelimbs and transition from alternating gait to synchronous flapping. In mammals, the spinal midline guidance molecule ephrin-B3 instructs the wiring that enables limb alternation, and its deletion leads to synchronous hopping gait. Here, we show that the ephrin-B3 protein in birds lacks several motifs present in other vertebrates, diminishing its affinity for the EphA4 receptor. The avian ephrin-B3 gene lacks an enhancer that drives midline expression and is missing in galliforms. The morphology and wiring at brachial levels of the chicken embryonic spinal cord resemble those of ephrin-B3 null mice. Dorsal midline decussation, evident in the mutant mouse, is apparent at the chick brachial level and is prevented by expression of exogenous ephrin-B3 at the roof plate. Our findings support a role for loss of ephrin-B3 function in shaping the avian brachial spinal cord circuitry and facilitating synchronous wing flapping.

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Sharp, Andrew A., and Sylvia Fromherz. "Optogenetic regulation of leg movement in midstage chick embryos through peripheral nerve stimulation." Journal of Neurophysiology 106, no. 5 (November 2011): 2776–82. http://dx.doi.org/10.1152/jn.00712.2011.

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Numerous disorders that affect proper development, including the structure and function of the nervous system, are associated with altered embryonic movement. Ongoing challenges are to understand in detail how embryonic movement is generated and to understand better the connection between proper movement and normal nervous system function. Controlled manipulation of embryonic limb movement and neuronal activity to assess short- and long-term outcomes can be difficult. Optogenetics is a powerful new approach to modulate neuronal activity in vivo. In this study, we have used an optogenetics approach to activate peripheral motor axons and thus alter leg motility in the embryonic chick. We used electroporation of a transposon-based expression system to produce ChIEF, a channelrhodopsin-2 variant, in the lumbosacral spinal cord of chick embryos. The transposon-based system allows for stable incorporation of transgenes into the genomic DNA of recipient cells. ChIEF protein is detectable within 24 h of electroporation, largely membrane-localized, and found throughout embryonic development in both central and peripheral processes. The optical clarity of thin embryonic tissue allows detailed innervation patterns of ChIEF-containing motor axons to be visualized in the living embryo in ovo, and pulses of blue light delivered to the thigh can elicit stereotyped flexures of the leg when the embryo is at rest. Continuous illumination can disrupt full extension of the leg during spontaneous movements. Therefore, our results establish an optogenetics approach to alter normal peripheral axon function and to probe the role of movement and neuronal activity in sensorimotor development throughout embryogenesis.

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Berki, �gnes Cs, Michael J. O'Donovan, and Mikl�s Antal. "Developmental expression of glycine immunoreactivity and its colocalization with gaba in the embryonic chick lumbosacral spinal cord." Journal of Comparative Neurology 362, no. 4 (November 27, 1995): 583–96. http://dx.doi.org/10.1002/cne.903620411.

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38

Vyklicky, L., L. Vyklický, V. Vlachová, J. Michl, and F. Vyskoc̆il. "Cobaltions block l-glutamate and l-aspartate-induced currents in cultured neurons from embryonic chick spinal cord." Neuroscience Letters 61, no. 3 (November 1985): 345–50. http://dx.doi.org/10.1016/0304-3940(85)90488-4.

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39

Wallace, James A., Permelia C. Allgood, Thomas J. Hoffman, Richard M. Mondragon, and Rolanda R. Maez. "Analysis of the change in number of serotonergic neurons in the chick spinal cord during embryonic development." Brain Research Bulletin 17, no. 3 (September 1986): 297–305. http://dx.doi.org/10.1016/0361-9230(86)90235-2.

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40

Loeb, J. A., T. S. Khurana, J. T. Robbins, A. G. Yee, and G. D. Fischbach. "Expression patterns of transmembrane and released forms of neuregulin during spinal cord and neuromuscular synapse development." Development 126, no. 4 (February 15, 1999): 781–91. http://dx.doi.org/10.1242/dev.126.4.781.

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We mapped the distribution of neuregulin and its transmembrane precursor in developing, embryonic chick and mouse spinal cord. Neuregulin mRNA and protein were expressed in motor and sensory neurons shortly after their birth and levels steadily increased during development. Expression of the neuregulin precursor was highest in motor and sensory neuron cell bodies and axons, while soluble, released neuregulin accumulated along early motor and sensory axons, radial glia, spinal axonal tracts and neuroepithelial cells through associations with heparan sulfate proteoglycans. Neuregulin accumulation in the synaptic basal lamina of neuromuscular junctions occurred significantly later, coincident with a reorganization of muscle extracellular matrix resulting in a relative concentration of heparan sulfate proteoglycans at endplates. These results demonstrate an early axonal presence of neuregulin and its transmembrane precursor at developing synapses and a role for heparan sulfate proteoglycans in regulating the temporal and spatial sites of soluble neuregulin accumulation during development.

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Antal, Miklós, Ágnes C. Berki, László Horváth, and Michael J. O'Donovan. "Development changes in the distribution of gamma-aminobutyric acid-immunoreactive neurons in the embryonic chick lumbosacral spinal cord." Journal of Comparative Neurology 343, no. 2 (May 8, 1994): 228–36. http://dx.doi.org/10.1002/cne.903430204.

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42

Du, Fu, Jean-Alain Chayvialle, and Paul Dubois. "Distribution and development of VIP immunoreactive neurons in the spinal cord of the embryonic and newly hatched chick." Journal of Comparative Neurology 268, no. 4 (February 22, 1988): 600–614. http://dx.doi.org/10.1002/cne.902680409.

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43

Mendelson, Bruce. "Chronic embryonic MK-801 exposure disrupts the somatotopic organization of cutaneous nerve projections in the chick spinal cord." Developmental Brain Research 82, no. 1-2 (October 1994): 152–66. http://dx.doi.org/10.1016/0165-3806(94)90158-9.

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44

Fournier le Ray, C., D. Renaud, and G. H. Le Douarin. "Change in motor neurone activity modifies the differentiation of a slow muscle in chick embryo." Development 106, no. 2 (June 1, 1989): 295–302. http://dx.doi.org/10.1242/dev.106.2.295.

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Slow-tonic anterior latissimus dorsi (ALD) muscle properties were studied following chronic spinal cord stimulation in chick embryo. Stimulation at a fast rhythm was applied from day 7, 8 or 10 of development until the end of embryonic life. When stimulation was applied from day 7 up to day 18 of development, ALD muscle exhibited at day 18 a large decrease in half time to peak of tetanic contraction, a large proportion of fast type II fibres and an increase in fast myosin light chain content as compared to control muscle. When stimulation started at day 8 of development, changes in properties of ALD muscle were reduced when compared to the previous experimental series. Indeed, no fast type II fibres were observed within the muscle, even when stimulation was prolongated until the 20th day of embryonic development. In addition, chronic stimulation at a fast rhythm initiated at day 10 of development did not modify ALD muscle differentiation. The present results indicate that a fast pattern of motor neurone activity can induce some slow-to-fast transformations of ALD muscle fibres. However, after the first week of embryonic life, ALD myotubes appeared refractory to these transformations. The possible mechanisms responsible for the transformation of slow myotubes and for their further loss of plasticity are discussed.

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45

Trupp, M., M. Rydén, H. Jörnvall, H. Funakoshi, T. Timmusk, E. Arenas, and C. F. Ibáñez. "Peripheral expression and biological activities of GDNF, a new neurotrophic factor for avian and mammalian peripheral neurons." Journal of Cell Biology 130, no. 1 (July 1, 1995): 137–48. http://dx.doi.org/10.1083/jcb.130.1.137.

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Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic polypeptide, distantly related to transforming growth factor-beta (TGF-beta), originally isolated by virtue of its ability to induce dopamine uptake and cell survival in cultures of embryonic ventral midbrain dopaminergic neurons, and more recently shown to be a potent neurotrophic factor for motorneurons. The biological activities and distribution of this molecule outside the central nervous system are presently unknown. We report here on the mRNA expression, biological activities and initial receptor binding characterization of GDNF and a shorter spliced variant termed GDNF beta in different organs and peripheral neurons of the developing rat. Both GDNF mRNA forms were found to be most highly expressed in developing skin, whisker pad, kidney, stomach and testis. Lower expression was also detected in developing skeletal muscle, ovary, lung, and adrenal gland. Developing spinal cord, superior cervical ganglion (SCG) and dorsal root ganglion (DRG) also expressed low levels of GDNF mRNA. Two days after nerve transection, GDNF mRNA levels increased dramatically in the sciatic nerve. Overall, GDNF mRNA expression was significantly higher in peripheral organs than in neuronal tissues. Expression of either GDNF mRNA isoform in insect cells resulted in the production of indistinguishable mature GDNF polypeptides. Purified recombinant GDNF promoted neurite outgrowth and survival of embryonic chick sympathetic neurons. GDNF produced robust bundle-like, fasciculated outgrowth from chick sympathetic ganglion explants. Although GDNF displayed only low activity on survival of newborn rat SCG neurons, this protein was found to increase the expression of vasoactive intestinal peptide and preprotachykinin-A mRNAs in cultured SCG neurons. GDNF also promoted survival of about half of the neurons in embryonic chick nodose ganglion and a small subpopulation of embryonic sensory neurons in chick dorsal root and rat trigeminal ganglia. Embryonic chick sympathetic neurons expressed receptors for GDNF with Kd 1-5 x 10(-9) M, as measured by saturation and displacement binding assays. Our findings indicate GDNF is a new neurotrophic factor for developing peripheral neurons and suggest possible non-neuronal roles for GDNF in the developing reproductive system.

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46

Houenou, Lucien J., Lanny J. Haverkamp, James L. McManaman, and Ronald W. Oppenheim. "The regulation of motoneuron survival and differentiation by putative muscle-derived neurotrophic agents: neuromuscular activity and innervation." Development 113, Supplement_2 (April 1, 1991): 149–55. http://dx.doi.org/10.1242/dev.113.supplement_2.149.

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The chronic blockade of neuromuscular activity is known to promote the survival of developing motoneurons in vivo in the chick, mouse and rat embryo. Increased survival in this situation may reflect an activity-dependent mechanism for the regulation of trophic factor production by target cells. To test this notion, we have examined motoneuron survival in vivo and choline acetyltransferase (ChAT) development in vitro following treatment of chick embryos and rat spinal cord cultures with partially purified skeletal muscle extracts derived from normally active, chronically paralyzed and aneural embryos, and from denervated postnatal chickens. Extracts from active and paralyzed chick embryos were equally effective in promoting motoneuron survival and ChAT activity. Aneural embryonic muscle extracts were slightly less effective in promoting motoneuron survival in vivo, but were not significantly different from control extracts in the in vitro ChAT assay. Denervated postnatal muscle extracts, however, were more effective in enhancing both motoneuron survival and ChAT activity. These data indicate that: (1) the promotion of motoneuron survival in vivo by activity blockade may not be mediated by an up-regulation of trophic factor synthesis in target cells; (2) postnatal innervation may regulate the production of putative muscle-derived neurotrophic factors; and (3) the synthesis or availability of trophic agents may be regulated differently in embryonic and postnatal muscle.

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47

Hamada, T. "Analysis of the structure and activity of a novel growth factor, SCDGF, isolated from the chick embryonic spinal cord." Neuroscience Research 38 (2000): S131. http://dx.doi.org/10.1016/s0168-0102(00)81631-4.

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Pirson, Marc, Stéphanie Debrulle, André Clippe, Frédéric Clotman, and Bernard Knoops. "Thioredoxin-2 Modulates Neuronal Programmed Cell Death in the Embryonic Chick Spinal Cord in Basal and Target-Deprived Conditions." PLOS ONE 10, no. 11 (November 5, 2015): e0142280. http://dx.doi.org/10.1371/journal.pone.0142280.

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49

Unsicker, Klaus, Carola Meier, Kerstin Krieglstein, Birgit M. Sartor, and Kathleen C. Flanders. "Expression, localization, and function of transforming growth factor-?s in embryonic chick spinal cord, hindbrain, and dorsal root ganglia." Journal of Neurobiology 29, no. 2 (February 1996): 262–76. http://dx.doi.org/10.1002/(sici)1097-4695(199602)29:2<262::aid-neu10>3.0.co;2-d.

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50

Thiriet, G., J. Kempf, and A. Ebel. "Distribution of cholinergic neurons in the chick spinal cord during embryonic development. Comparison of ChAT immunocytochemistry with AChE histochemistry." International Journal of Developmental Neuroscience 10, no. 5 (October 1992): 459–66. http://dx.doi.org/10.1016/0736-5748(92)90037-z.

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