Structures of filum terminale and characteristics of ependymal cells of its central canal in rats

2019 ◽  
Vol 1707 ◽  
pp. 208-215
Author(s):  
Norihiko Nakano ◽  
Kenji Kanekiyo ◽  
Yoshihiro Yamada ◽  
Masahiro Tamachi ◽  
Yoshihisa Suzuki ◽  
...  
2021 ◽  
Author(s):  
R. Chevreau ◽  
H Ghazale ◽  
C Ripoll ◽  
C Chalfouh ◽  
Q Delarue ◽  
...  

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.


1977 ◽  
Vol 46 (5) ◽  
pp. 609-617 ◽  
Author(s):  
W. James Gardner ◽  
Herbert S. Bell ◽  
Pete N. Poolos ◽  
Donald F. Dohn ◽  
Marta Steinberg

✓ The clinical course of 12 patients who underwent terminal ventriculostomy for syringomyelia is presented. Opening the central canal at the tip of the conus medullaris is a relatively benign procedure that improves the symptoms of syringomyelia and syringobulbia. This canal normally terminates at the tip of the conus, but in each of the 12 surgical specimens it continued into the filum terminale for distances up to 8 cm. In most cases the tip of the conus was located more caudally than normal, indicating some degree of tethering in fetal life. This belief is supported by the fact that the newborn, whose conus is tethered to a lipoma at the sacral level, may develop syringomyelia in adult life.


1989 ◽  
Vol 71 (2) ◽  
pp. 239-243 ◽  
Author(s):  
Kesava K. V. Reddy ◽  
Marc R. Del Bigio ◽  
Garnette R. Sutherland

✓ Although posttraumatic syringomyelia is a well-established clinicopathological entity, there is a paucity of information on the ultrastructural features of this condition. This study documents the light and electron microscopic features of posttraumatic syringes obtained from two patients who underwent surgical cordectomy. The syringes were lined largely by cell processes of astrocytes. Small regions near the caudal end were lined by flattened ependymal cells that lacked surface specializations. These were thought to represent remnants of the central canal ependyma. The ultrastructural appearance of the syrinx was similar to that of the communicating syringomyelia as well as the periventricular changes that accompany hydrocephalus. The authors conclude that the changes represent the nonspecific sequelae of a distensile force within the syrinx cavity.


1980 ◽  
Vol 53 (4) ◽  
pp. 528-532 ◽  
Author(s):  
Vijayashekara S. Murthy ◽  
Dhirendra H. Deshpande

✓ Lumbar thecoperitoneal shunting was carried out in patients with communicating hydrocephalus due to long-standing tuberculous meningitis. At the time of this surgical procedure, the filum terminale was excised to achieve filum terminostomy. The central canal of the excised filum terminale in seven hydrocephalic children and an equal number from control cases was studied histologically. These observations indicate that the central canal of the filum terminale dilates in communicating hydrocephalus, and the dilatation is proportionate to the lateral ventricular enlargement.


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 ◽  
...  

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.


2018 ◽  
Vol 29 (2) ◽  
pp. 199-207 ◽  
Author(s):  
Jichao Ye ◽  
Yi Qin ◽  
Yong Tang ◽  
Mengjun Ma ◽  
Peng Wang ◽  
...  

OBJECTIVEThe aim of this work was to investigate the effects of methylprednisolone on the proliferation of endogenous neural stem cells (ENSCs) in nonhuman primates with spinal cord injury (SCI).METHODSA total of 14 healthy cynomolgus monkeys (Macaca fascicularis) (4–5 years of age) were randomly divided into 3 groups: the control group (n = 6), SCI group (n = 6), and methylprednisolone therapy group (n = 2). Only laminectomy was performed in the control animals at T-10. SCI was induced in monkeys using Allen’s weight-drop method (50 mm × 50 g) to injure the posterior portion of the spinal cord at T-10. In the methylprednisolone therapy group, monkeys were intravenously infused with methylprednisolone (30 mg/kg) immediately after SCI. All animals were intravenously infused with 5-bromo-2-deoxyuridine (BrdU) (50 mg/kg/day) for 3 days prior to study end point. The small intestine was dissected for immunohistochemical examination. After 3, 7, and 14 days, the spinal cord segments of the control and SCI groups were dissected to prepare frozen and paraffin sections. The proliferation of ENSCs was evaluated using BrdU and nestin immunofluorescence staining.RESULTSHistological examination showed that a larger number of mucosa epithelial cells in the small intestine of all groups were BrdU positive. Nestin-positive ependymal cells are increased around the central canal after SCI. After 3, 7, and 14 days of SCI, BrdU-positive ependymal cells in the SCI group were significantly increased compared with the control group, and the percentage of BrdU-positive cells in the left/right ventral horns and dorsal horn was significantly higher than that of the control group. Seven days after SCI, the percentages of both BrdU-positive ependymal cells around the central canal and BrdU– and nestin–double positive cells in the left/right ventral horns and dorsal horn were significantly lower in the methylprednisolone therapy group than in the SCI group.CONCLUSIONSWhile ENSCs proliferate significantly after SCI in nonhuman primates, methylprednisolone can inhibit the proliferation of ependymal cells after SCI.


Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1680
Author(s):  
Francesco Fabozzi ◽  
Silvia Ceccanti ◽  
Antonella Cacchione ◽  
Giovanna Stefania Colafati ◽  
Andrea Carai ◽  
...  

Primary central nervous system (CNS) tumors represent the most common solid tumors in childhood. Ependymomas arise from ependymal cells lining the wall of ventricles or central canal of spinal cord and their occurrence outside the CNS is extremely rare, published in the literature as case reports or small case series. We present two cases of extra-CNS myxopapillary ependymomas treated at our institution in the past three years; both cases originate in the sacrococcygeal region and were initially misdiagnosed as epidermoid cyst and germ cell tumor, respectively. The first case, which arose in a 9-year-old girl, was treated with a surgical excision in two stages, due to the non-radical manner of the first operation; no recurrence was observed after two years of follow-up. The other case was a 12-year-old boy who was treated with a complete resection and showed no evidence of recurrence at one-year follow-up. In this paper, we report our experience in treating an extremely rare disease that lacks a standardized approach to diagnosis, treatment and follow-up; in addition, we perform a literature review of the past 35 years.


Author(s):  
Jill K. Frey ◽  
Aileen Chen ◽  
R. David Heathcote

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.


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