Ependymal morphogenesis in a simple vertebrate spinal cord

1993 ◽  
Vol 51 ◽  
pp. 424-425
Author(s):  
Jill K. Frey ◽  
Aileen Chen ◽  
R. David Heathcote
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Single Layer ◽  
Central Canal ◽  
Floor Plate ◽  
Turn Of The Century ◽  
Ependymal Cells ◽  
Embryonic Spinal Cord ◽  
Developing Spinal Cord ◽  
Tyrosine Hydroxylase Immunocytochemistry

All cells of the spinal cord originate from the single layer of neuroepithelium that lines the central canal. Since the turn of the century, it has been known that a subclass of these ependymal cells can differentiate into neurons and extend cytoplasmic projections and cilia into the central canal. We have recently used tyrosine hydroxylase immunocytochemistry to identify a catecholaminergic subpopulation of cerebrospinal fluid (CSF) contacting ependymal neurons in the developing spinal cord of the frog Xenopus laevis (Fig. 1). The interneurons are located in the floor plate region of the spinal cord and have axons that extend rostrally toward the hindbrain. During the morphogenesis of the catecholaminergic population of cells, two longitudinal columns gradually appear and then rapidly “converge” at the ventral midline. Transverse sections of embryonic spinal cord (see Fig. 1) showed that the cell bodies decreased in size and underwent changes in shape, number and position within the spinal cord.

scholarly journals Olig2-positive progenitors in the embryonic spinal cord give rise not only to motoneurons and oligodendrocytes, but also to a subset of astrocytes and ependymal cells

2006 ◽  
Vol 293 (2) ◽  
pp. 358-369 ◽  
Author(s):  
Noritaka Masahira ◽  
Hirohide Takebayashi ◽  
Katsuhiko Ono ◽  
Keisuke Watanabe ◽  
Lei Ding ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ependymal Cells ◽  
Embryonic Spinal Cord

scholarly journals Reaction of ependymal cells to spinal cord injury: a potential role for oncostatin pathway and microglial cells

2021 ◽  
Author(s):  
R. Chevreau ◽  
H Ghazale ◽  
C Ripoll ◽  
C Chalfouh ◽  
Q Delarue ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Glial Cells ◽  
Mapk Signaling ◽  
Central Canal ◽  
Microglial Cells ◽  
Ependymal Cells ◽  
Rna Profiling ◽  
Cord Injury

AbstractEpendymal cells with stem cell properties reside in the adult spinal cord around the central canal. They rapidly activate and proliferate after spinal cord injury, constituting a source of new cells. They produce neurons and glial cells in lower vertebrates but they mainly generate glial cells in mammals. The mechanisms underlying their activation and their glial-biased differentiation in mammals remain ill-defined. This represents an obstacle to control these cells. We addressed this issue using RNA profiling of ependymal cells before and after injury. We found that these cells activate STAT3 and ERK/MAPK signaling during injury and downregulate cilia-associated genes and FOXJ1, a central transcription factor in ciliogenesis. Conversely, they upregulate 510 genes, six of them more than 20 fold, namely Crym, Ecm1, Ifi202b, Nupr1, Rbp1, Thbs2 and Osmr. OSMR is the receptor for the inflammatory cytokine oncostatin (OSM) and we studied its regulation and role using neurospheres derived from ependymal cells. We found that OSM induces strong OSMR and p-STAT3 expression together with proliferation reduction and astrocytic differentiation. Conversely, production of oligodendrocyte-lineage OLIG1+ cells was reduced. OSM is specifically expressed by microglial cells and was strongly upregulated after injury. We observed microglial cells apposed to ependymal cells in vivo and co-cultures experiments showed that these cells upregulate OSMR in neurosphere cells. Collectively, these results support the notion that microglial cells and OSMR/OSM pathway regulate ependymal cells in injury. In addition, the generated high throughput data provides a unique molecular resource to study how ependymal cell react to spinal cord lesion.

Evaluation of the central canal of the spinal cord in experimentally induced hydrocephalus

1978 ◽  
Vol 48 (6) ◽  
pp. 970-974 ◽  
Author(s):  
A. Everette James ◽  
William J. Flor ◽  
Gary R. Novak ◽  
Ernst-Peter Strecker ◽  
Barry Burns
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Experimental Model ◽  
Alternative Pathway ◽  
Central Canal ◽  
Communicating Hydrocephalus ◽  
Csf Flow ◽  
Content Type ◽  
Histological Appearance ◽  
Fine Print

✓ The central canal of the spinal cord has been proposed as a significant compensatory alternative pathway of cerebrospinal fluid (CSF) flow in hydrocephalus. Ten dogs were made hydrocephalic by a relatively atraumatic experimental model that simulates the human circumstance of chronic communicating hydrocephalus. The central canal was studied by histopathology and compared with 10 normal control dogs. In both groups the central canal of the spinal cord was normal in size, configuration, and histological appearance. In this experimental model dilatation of the canal and increased movement of CSF does not appear to be a compensatory alternative pathway.

The distribution of non-synaptic intercellular junctions during neurone differentiation in the developing spinal cord of the clawed toad

Development ◽  
1975 ◽  
Vol 33 (2) ◽  
pp. 403-417
Author(s):  
Brian P. Hayes ◽  
Alan Roberts
Keyword(s):  
Spinal Cord ◽  
Gap Junctions ◽  
Neural Differentiation ◽  
Electrical Coupling ◽  
Intercellular Junctions ◽  
Ependymal Cells ◽  
Freedom Of Movement ◽  
Ventricular Cells ◽  
Vertebrate Embryos ◽  
Developing Spinal Cord

The distribution of intercellular junctions, other than synapses and their precursors, has beendescribed in the developing spinal cord of Xenopus laevis between the neurula andfree swimming tadpole stages. At the neurocoel, ventricular cells are joined in the apical contactzone by a sequence of junctions which usually has one or more intermediate junctions but often also includes close appositions, gap junctions and desmosomes. This apical complex is more diverse than that reported in other vertebrate embryos and between ependymal cells in the adult central nervous system. Gap junctions are also found between ventricular cells and their processes near the external cord surface. However, no other special junctions occur in this location under the basementlamella which surrounds the cord. Punctate intermediate junctions are generally distributed between undifferentiated and differentiating cells and their processes but were not found in neuropil after stage 28. These results are discussed in relation to cell movements during neural differentiation, possible effects on the freedom of movement of ions and molecules through extracellular pathways in the embryo, and possible intercytoplasmic pathways via gap junctions which may be responsible for the physiologically observed electrical coupling between neural tube cells.

scholarly journals Syringohydromyelia associated to therapeutic procedures for severe forms of neurocysticercoses: case report

2004 ◽  
Vol 62 (3b) ◽  
pp. 885-888
Author(s):  
Donizeti Honorato ◽  
Wilson Borges ◽  
Antonio Augusto Roth Vargas ◽  
Ricardo Ramina
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Case Report ◽  
Posterior Fossa ◽  
Central Canal ◽  
Severe Form ◽  
Surgical Decompression ◽  
Therapeutic Procedures ◽  
Surgical Treatments ◽  
Progressive Paraparesis

Syringohydromyelia is defined as a longitudinal dilatation of the central canal of the spinal cord with accumulated cerebrospinal fluid. This condition may cause neurologic deficits when the cavity enlarges and compresses the spinal cord. We present the case of a 33 years-old female with progressive paraparesis caused by syringohydromyelia. This patient underwent previously multiple clinical and surgical treatments for severe form of neurocysticercosis. Surgical decompression of the posterior fossa and syringostomy resolved the neurologic symptoms. The possibility of syringohydromyelia should be considered in the case of patients who have previously undergone surgical and clinical treatment for severe form of neurocysticercosis.

The Origins of Syringomyelia: Numerical Models of Fluid/Structure Interactions in the Spinal Cord

2005 ◽  
Vol 127 (7) ◽  
pp. 1099-1109 ◽  
Author(s):  
C. D. Bertram ◽  
A. R. Brodbelt ◽  
M. A. Stoodley
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Wave Propagation ◽  
Numerical Models ◽  
Scar Tissue ◽  
Central Canal ◽  
Radial Wave ◽  
Wave Speeds ◽  
Arterial Pulsation ◽  
Elastic Cord

A two-dimensional axi-symmetric numerical model is constructed of the spinal cord, consisting of elastic cord tissue surrounded by aqueous cerebrospinal fluid, in turn surrounded by elastic dura. The geometric and elastic parameters are simplified but of realistic order, compared with existing measurements. A distal reflecting site models scar tissue formed by earlier trauma to the cord, which is commonly associated with syrinx formation. Transients equivalent to both arterial pulsation and percussive coughing are used to excite wave propagation. Propagation is investigated in this model and one with a central canal down the middle of the cord tissue, and in further idealized versions of it, including a model with no cord, one with a rigid cord, one with a rigid dura, and a double-length untapered variant of the rigid-dura model. Analytical predictions for axial and radial wave-speeds in these different situations are compared with, and used to explain, the numerical outcomes. We find that the anatomic circumstances of the spinal cerebrospinal fluid cavity probably do not allow for significant wave steepening phenomena. The results indicate that wave propagation in the real cord is set by the elastic properties of both the cord tissue and the confining dura mater, fat, and bone. The central canal does not influence the wave propagation significantly.

scholarly journals Multiple steps mediate ventricular layer attrition to form the adult mouse spinal cord central canal

2019 ◽  
Author(s):  
Marco A. Cañizares ◽  
Aida Rodrigo Albors ◽  
Gail Singer ◽  
Nicolle Suttie ◽  
Metka Gorkic ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Proliferation ◽  
Expression Patterns ◽  
Central Canal ◽  
Floor Plate ◽  
Cell Potential ◽  
Proliferation Markers ◽  
Tissue Organization ◽  
Stem Cell Potential ◽  
Adult Spinal Cord

AbstractThe ventricular layer of the spinal cord is remodelled during embryonic development and ultimately forms the adult central canal, which retains neural stem cell potential. This anatomical transformation involves the process of dorsal collapse, however, accompanying changes in tissue organization and cell behaviour as well as the origin of cells contributing to the adult central canal are not well understood. Here we describe sequential localised cell rearrangements which contribute to the gradual attrition of the spinal cord ventricular layer during development. This includes local breakdown of the pseudostratified organisation of the dorsal ventricular layer prefiguring dorsal collapse and evidence for a new phenomenon, ventral dissociation, during which the ventral-most floor plate cells separate from a subset that are retained in the central canal. Using cell proliferation markers and cell-cycle reporter mice, we further show that following dorsal collapse, ventricular layer attrition involves an overall reduction in cell proliferation, characterised by an intriguing increase in the percentage of cells in G1/S. In contrast, programmed cell death does not contribute to ventricular layer remodelling. By analysing transcript and protein expression patterns associated with key signalling pathways, we provide evidence for a gradual decline in ventral sonic hedgehog activity and an accompanying ventral expansion of initial dorsal bone morphogenetic protein signalling, which comes to dominate the forming central canal. This study identifies multiple steps that contribute to spinal cord ventricular layer attrition and adds to increasing evidence for the heterogenous origin of the adult spinal cord central canal, which includes cells from the floor plate and the roof plate as well as ventral progenitor domain.

scholarly journals The Structure of the Spinal Cord Ependymal Region in Adult Humans Is a Distinctive Trait among Mammals

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2235
Author(s):  
Alejandro Torrillas de la Cal ◽  
Beatriz Paniagua-Torija ◽  
Angel Arevalo-Martin ◽  
Christopher Guy Faulkes ◽  
Antonio Jesús Jiménez ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Small Groups ◽  
Central Canal ◽  
Ependymal Cells ◽  
Injured Spinal Cord ◽  
Heterocephalus Glaber ◽  
Mole Rat ◽  
Naked Mole Rat ◽  
Adult Humans ◽  
Human Trait

In species that regenerate the injured spinal cord, the ependymal region is a source of new cells and a prominent coordinator of regeneration. In mammals, cells at the ependymal region proliferate in normal conditions and react after injury, but in humans, the central canal is lost in the majority of individuals from early childhood. It is replaced by a structure that does not proliferate after damage and is formed by large accumulations of ependymal cells, strong astrogliosis and perivascular pseudo-rosettes. We inform here of two additional mammals that lose the central canal during their lifetime: the Naked Mole-Rat (NMR, Heterocephalus glaber) and the mutant hyh (hydrocephalus with hop gait) mice. The morphological study of their spinal cords shows that the tissue substituting the central canal is not similar to that found in humans. In both NMR and hyh mice, the central canal is replaced by tissue reminiscent of normal lamina X and may include small groups of ependymal cells in the midline, partially resembling specific domains of the former canal. However, no features of the adult human ependymal remnant are found, suggesting that this structure is a specific human trait. In order to shed some more light on the mechanism of human central canal closure, we provide new data suggesting that canal patency is lost by delamination of the ependymal epithelium, in a process that includes apical polarity loss and the expression of signaling mediators involved in epithelial to mesenchymal transitions.

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