scholarly journals Wnt produced by stretched roof-plate cells is required for the promotion of cell proliferation around the central canal of the spinal cord

Development ◽  
2019 ◽  
Vol 146 (2) ◽  
pp. dev159343 ◽  
Author(s):  
Takuma Shinozuka ◽  
Ritsuko Takada ◽  
Shosei Yoshida ◽  
Shigenobu Yonemura ◽  
Shinji Takada
Keyword(s):  
Spinal Cord ◽  
Cell Proliferation ◽  
Central Canal ◽  
Roof Plate

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 Morphological and Functional Changes of Roof Plate Cells in Spinal Cord Development

2021 ◽  
Vol 9 (3) ◽  
pp. 30
Author(s):  
Takuma Shinozuka ◽  
Shinji Takada
Keyword(s):  
Spinal Cord ◽  
Neural Crest ◽  
Morphological Changes ◽  
Neural Crest Cells ◽  
Central Canal ◽  
Ependymal Cells ◽  
Morphological Transformation ◽  
Functional Changes ◽  
Median Septum ◽  
Roof Plate

The most dorsal region, or roof plate, is the dorsal organizing center of developing spinal cord. This region is also involved in development of neural crest cells, which are the source of migratory neural crest cells. During early development of the spinal cord, roof plate cells secrete signaling molecules, such as Wnt and BMP family proteins, which regulate development of neural crest cells and dorsal spinal cord. After the dorso-ventral pattern is established, spinal cord dynamically changes its morphology. With this morphological transformation, the lumen of the spinal cord gradually shrinks to form the central canal, a cavity filled with cerebrospinal fluid that is connected to the ventricular system of the brain. The dorsal half of the spinal cord is separated by a glial structure called the dorsal (or posterior) median septum. However, underlying mechanisms of such morphological transformation are just beginning to be understood. Recent studies reveal that roof plate cells dramatically stretch along the dorso-ventral axis, accompanied by reduction of the spinal cord lumen. During this stretching process, the tips of roof plate cells maintain contact with cells surrounding the shrinking lumen, eventually exposed to the inner surface of the central canal. Interestingly, Wnt expression remains in stretched roof plate cells and activates Wnt/β-catenin signaling in ependymal cells surrounding the central canal. Wnt/β-catenin signaling in ependymal cells promotes proliferation of neural progenitor and stem cells in embryonic and adult spinal cord. In this review, we focus on the role of the roof plate, especially that of Wnt ligands secreted by roof plate cells, in morphological changes occurring in the spinal cord.

scholarly journals Crumbs2 mediates ventricular layer remodelling to form the spinal cord central canal

PLoS Biology ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. e3000470 ◽  
Author(s):  
Christine M. Tait ◽  
Kavitha Chinnaiya ◽  
Elizabeth Manning ◽  
Mariyam Murtaza ◽  
John-Paul Ashton ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Canal

Anatomical and physiological studies of the gray matter surrounding the spinal cord central canal

1983 ◽  
Vol 220 (3) ◽  
pp. 321-335 ◽  
Author(s):  
Richard L. Nahin ◽  
Anne M. Madsen ◽  
Glenn J. Giesler
Keyword(s):  
Spinal Cord ◽  
Gray Matter ◽  
Central Canal ◽  
Physiological Studies

Histopathology of experimental hematomyelia

1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher
Keyword(s):  
Spinal Cord ◽  
Tissue Injury ◽  
Central Canal ◽  
Microglial Cells ◽  
Neurological Deficits ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Cellular Debris ◽  
Dorsal Columns

✓ The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 µl blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.

The Central Canal of the Spinal Cord: Ultrasonic Identification

Radiology ◽  
1985 ◽  
Vol 155 (2) ◽  
pp. 535-536
Author(s):  
Berta M. Montalvo ◽  
Paul H. Skaggs
Keyword(s):  
Spinal Cord ◽  
Central Canal

scholarly journals Natural loss of function of ephrin-B3 shapes spinal flight circuitry in birds

2021 ◽  
Vol 7 (24) ◽  
pp. eabg5968
Author(s):  
Baruch Haimson ◽  
Oren Meir ◽  
Reut Sudakevitz-Merzbach ◽  
Gerard Elberg ◽  
Samantha Friedrich ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Mutant Mouse ◽  
Loss Of Function ◽  
Dorsal Midline ◽  
Roof Plate ◽  
Embryonic Spinal Cord ◽  
Guidance Molecule

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.

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.

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