scholarly journals Differentiation of choroid plexus ependymal cells into astrocytes after grafting into the pre-lesioned spinal cord in mice

Glia ◽  
2001 ◽  
Vol 36 (3) ◽  
pp. 364-374 ◽  
Author(s):  
Masaaki Kitada ◽  
Shushovan Chakrabortty ◽  
Naoya Matsumoto ◽  
Masanori Taketomi ◽  
Chizuka Ide
Keyword(s):  
Spinal Cord ◽  
Choroid Plexus ◽  
Ependymal Cells

Grafting of Choroid Plexus Ependymal Cells Promotes the Growth of Regenerating Axons in the Dorsal Funiculus of Rat Spinal Cord: A Preliminary Report

2001 ◽  
Vol 167 (2) ◽  
pp. 242-251 ◽  
Author(s):  
Chizuka Ide ◽  
Masaaki Kitada ◽  
Shushovan Chakrabortty ◽  
Masanori Taketomi ◽  
Naoya Matsumoto ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Choroid Plexus ◽  
Preliminary Report ◽  
Ependymal Cells ◽  
Rat Spinal Cord ◽  
Dorsal Funiculus

scholarly journals LOCALIZATION OF THE VIRUS AND PATHOGENESIS OF EPIDEMIC POLIOMYELITIS

1914 ◽  
Vol 20 (3) ◽  
pp. 249-268 ◽  
Author(s):  
Simon Flexner ◽  
Harold L. Amoss
Keyword(s):  
Spinal Cord ◽  
Choroid Plexus ◽  
Horse Serum ◽  
Lymphatic Invasion ◽  
Immune Serum ◽  
The Body ◽  
Ependymal Cells ◽  
Intracerebral Injection ◽  
Aseptic Inflammation ◽  
Set Up

The virus of poliomyelitis is capable of penetrating the retina without producing apparent injury, to reach the central nervous organs. The virus injected into the blood is deposited promptly in the spleen and bone marrow, but not in the kidneys, spinal cord, or brain. Notwithstanding the affinity which the nervous tissues possess for the virus, it is not removed from the blood by the spinal cord and brain until the choroid plexus and blood vessels have suffered injury. The intervertebral ganglia remove the virus from the blood earlier than do the spinal cord and brain. An aseptic inflammation produced by an intraspinous injection of horse serum facilitates and insures the passage of the virus to the central nervous organs, and the production of paralysis. The unaided virus, even when present in large amounts, passes inconstantly from the blood to the substance of the spinal cord and brain. When the virus within the blood fails to gain access to the central nervous organs, and to set up paralysis, it is destroyed by the body, in course of which destruction it undergoes, as a result of the action of the spleen and, perhaps, other organs, diminution of virulence. The histological lesions that follow the intravenous injections of the virus in some but not in all cases differ from those which result from intraneural modes of infection. In escaping from the blood into the spinal cord and brain, the virus causes a lymphatic invasion of the choroid plexus and widespread perivascular infiltration, and from the latter cellular invasions enter the nervous tissues. A similar lymphoid infiltration of the choroid plexus may arise also from an intracerebral injection of the virus. The histological lesions present in the central nervous organs in human cases of poliomyelitis correspond to those that arise from the intraneural method of infection in the monkey. The virus in transit from the blood through the cerebrospinal fluid to the substance of the spinal cord and brain is capable of being neutralized by intraspinous injection of immune serum, whereby the production of paralysis is averted. Carmin in a sterile and finely divided state introduced into the meninges and ventricles sets up an aseptic inflammation, but is quickly taken up by cells, including ependymal cells. When an aseptic inflammation has been previously established by means of horse serum, or when the nervous tissues are already injured by the poliomyelitic virus, the pigment appears to enter the ependymal cells more freely. The experiments described support the view that infection in epidemic poliomyelitis in man is local and neural, and by way of the lymphatics, and not general and by way of the blood. Hence they uphold the belief that the infection atrium is the upper respiratory mucous membrane.

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

Proliferation and Differentiation of Ependymal Cells after Transection of the Carp Spinal Cord

1997 ◽  
Vol 14 (2) ◽  
pp. 331-338 ◽  
Author(s):  
Hajime Yamada ◽  
Toshihiko Miyake ◽  
Tadahisa Kitamura
Keyword(s):  
Spinal Cord ◽  
Ependymal Cells ◽  
Proliferation And Differentiation

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.

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.

Altered pHi regulation and Na+/HCO3− transporter activity in choroid plexus of cilia-defective Tg737orpk mutant mouse

2007 ◽  
Vol 292 (4) ◽  
pp. C1409-C1416 ◽  
Author(s):  
Boglarka Banizs ◽  
Peter Komlosi ◽  
Mark O. Bevensee ◽  
Erik M. Schwiebert ◽  
Phillip D. Bell ◽  
...  
Keyword(s):  
Ion Transport ◽  
Choroid Plexus ◽  
Perinatal Period ◽  
Ependymal Cells ◽  
Intracellular Camp ◽  
Transport Activity ◽  
Wild Type ◽  
Choroid Plexus Epithelium ◽  
Fluid Movement ◽  
Camp Levels

Tg737 orpk mice have defects in cilia assembly and develop hydrocephalus in the perinatal period of life. Hydrocephalus is progressive and is thought to be initiated by abnormal ion and water transport across the choroid plexus epithelium. The pathology is further aggravated by the slow and disorganized beating of motile cilia on ependymal cells that contribute to decreased cerebrospinal fluid movement through the ventricles. Previously, we demonstrated that the hydrocephalus phenotype is associated with a marked increase in intracellular cAMP levels in choroid plexus epithelium, which is known to have regulatory effects on ion and fluid movement in many secretory epithelia. To evaluate whether the hydrocephalus in Tg737 orpk mutants is associated with defects in ion transport, we compared the steady-state pHi and Na+-dependent transport activities of isolated choroid plexus epithelium tissue from Tg737 orpk mutant and wild-type mice. The data indicate that Tg737 orpk mutant choroid plexus epithelium have lower pHi and higher Na+-dependent HCO3− transport activity compared with wild-type choroid plexus epithelium. In addition, wild-type choroid plexus epithelium could be converted to a mutant phenotype with regard to the activity of Na+-dependent HCO3− transport by addition of dibutyryl-cAMP and mutant choroid plexus epithelium toward the wild-type phenotype by inhibiting PKA activity with H-89. Together, these data suggest that cilia have an important role in regulating normal physiology of choroid plexus epithelium and that ciliary dysfunction in Tg737 orpk mutants disrupts a signaling pathway leading to elevated intracellular cAMP levels and aberrant regulation of pHi and ion transport activity.

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