Teasing of Ventral Spinal Cord White Matter Fibers for the Analysis of Central Nervous System Nodes of Ranvier

Author(s):  
Andrew A. Jarjour ◽  
Diane L. Sherman
1970 ◽  
Vol 7 (5) ◽  
pp. 435-447 ◽  
Author(s):  
K. M. Charlton ◽  
K. R. Pierce ◽  
R. W. Storts ◽  
C. H. Bridges

Twenty-two goats were poisoned with daily oral doses of ground coyotillo fruits and were killed at various times after the first day of dosing. The morphologic features and distribution of lesions in the central nervous system were studied by light microscopy. An axonal dystrophy occurred in several of the goats given high daily doses. Swellings occurred along axons of Purkinje cells in the cerebellum and in the white matter of the spinal cord. There was a fairly close correlation between the occurrence of clinical signs suggestive of the neocerebellar syndrome and the occurrence and distribution of lesions in the cerebellum.


1999 ◽  
Vol 73 (1) ◽  
pp. 801-804 ◽  
Author(s):  
Nadine Jarousse ◽  
Ekaterina G. Viktorova ◽  
Evgeny V. Pilipenko ◽  
Vadim I. Agol ◽  
Michel Brahic

ABSTRACT The DA strain of Theiler’s virus causes a persistent and demyelinating infection of the white matter of spinal cord, whereas the GDVII strain causes a fatal gray-matter encephalomyelitis. Studies with recombinant viruses showed that this difference in phenotype is controlled mainly by the capsid. However, conflicting results regarding the existence of determinants of persistence in the capsid of the GDVII strain have been published. Here we show that a GDVII virus whose neurovirulence has been attenuated by an insertion in the 5′ noncoding region does not persist in the central nervous systems of mice. Furthermore, this virus infects the gray matter efficiently, but not the white matter. These results confirm the absence of determinants of persistence in the GDVII capsid. They suggest that the DA capsid controls persistence by allowing the virus to infect cells in the white matter of the spinal cord.


Neuron ◽  
2013 ◽  
Vol 78 (3) ◽  
pp. 469-482 ◽  
Author(s):  
Keiichiro Susuki ◽  
Kae-Jiun Chang ◽  
Daniel R. Zollinger ◽  
Yanhong Liu ◽  
Yasuhiro Ogawa ◽  
...  

2008 ◽  
Vol 4 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Xiaoqin Zhu ◽  
Robert A. Hill ◽  
Akiko Nishiyama

NG2 cells represent a unique glial cell population that is distributed widely throughout the developing and adult CNS and is distinct from astrocytes, mature oligodendrocytes and microglia. The ability of NG2 cells to differentiate into myelinating oligodendrocytes has been documented in vivo and in vitro. We reported recently that NG2 cells in the forebrain differentiate into myelinating oligodendrocytes but into a subpopulation of protoplasmic astrocytes (Zhu et al., 2008). However, the in vivo fate of NG2 cells in the spinal cord and cerebellum has remained unknown. To investigate the fate of NG2 cells in caudal central nervous system (CNS) regions in vivo, we examined the phenotype of cells that express EGFP in mice that are double transgenic for NG2CreBAC and the Cre reporter Z/EG. The fate of NG2 cells can be studied in these mice by permanent expression of EGFP in cells that have undergone Cre-mediated recombination in NG2 cells. We find that NG2 cells give rise to oligodendrocytes in both gray and white matter of the spinal cord and cerebellum, and to protoplasmic astrocytes in the gray matter of the spinal cord. However, NG2 cells do not give rise to astrocytes in the white matter of the spinal cord and cerebellum. These observations indicate that NG2 cells serve as precursor cells for oligodendrocytes and a subpopulation of protoplasmic astrocytes throughout the rostrocaudal axis of the CNS.


Development ◽  
1964 ◽  
Vol 12 (3) ◽  
pp. 491-499
Author(s):  
R. T. Sims

Sterzi (1904) studied the blood vessels of the spinal cord in the embryos and adults of a comprehensive series of chordates. He suggested that the formation of new blood vessels in the developing neural tube is controlled by local variations in the metabolic activity of the nerve cells, and that the grey matter of the adult central nervous system is more vascular than the white matter because it is functionally more active. A marked increase in the vascularity of the central nervous system during development has been demonstrated by quantitative observations on rats (Craigie, 1925), guinea-pigs (Petren, 1938), mice (Gyllensten, 1959a), chickens (Williams, 1937) and toads (Sims, 1961). This increase is associated with the maturation of the neurones and no experiments have been performed which separate the production of new blood vessels and the differentiation of these cells. Experimental conditions which prevent the increased vascularity of the mammalian central nervous system during development also prevent differentiation of the neurones.


2003 ◽  
Vol 77 (22) ◽  
pp. 12252-12265 ◽  
Author(s):  
Moses Rodriguez ◽  
Laurie J. Zoecklein ◽  
Charles L. Howe ◽  
Kevin D. Pavelko ◽  
Jeff D. Gamez ◽  
...  

ABSTRACT We evaluated the role of gamma interferon (IFN-γ) in protecting neurons from virus-induced injury following central nervous system infection. IFN-γ−/− and IFN-γ+/+ mice of the resistant major histocompatibility complex (MHC) H-2b haplotype and intracerebrally infected with Theiler's murine encephalomyelitis virus (TMEV) cleared virus infection from anterior horn cell neurons. IFN-γ+/+ H-2b mice also cleared virus from the spinal cord white matter, whereas IFN-γ−/− H-2b mice developed viral persistence in glial cells of the white matter and exhibited associated spinal cord demyelination. In contrast, infection of IFN-γ−/− mice of the susceptible H-2q haplotype resulted in frequent deaths and severe neurologic deficits within 16 days of infection compared to the results obtained for controls. Morphologic analysis demonstrated severe injury to spinal cord neurons in IFN-γ−/− H-2q mice during early infection. More virus RNA was detected in the brain and spinal cord of IFN-γ−/− H-2q mice than in those of control mice at 14 and 21 days after TMEV infection. Virus antigen was localized predominantly to anterior horn cells in infected IFN-γ−/− H-2q mice. IFN-γ deletion did not affect the humoral response directed against the virus. However, the level of expression of CD4, CD8, class I MHC, or class II MHC in the central nervous system of IFN-γ−/− H-2q mice was lower than those in IFN-γ+/+ H-2q mice. Finally, in vitro analysis of virus-induced death in NSC34 cells and spinal motor neurons showed that IFN-γ exerted a neuroprotective effect in the absence of other aspects of the immune response. These data support the hypothesis that IFN-γ plays a critical role in protecting spinal cord neurons from persistent infection and death.


2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.


1963 ◽  
Vol 44 (3) ◽  
pp. 475-480 ◽  
Author(s):  
R. Grinberg

ABSTRACT Radiologically thyroidectomized female Swiss mice were injected intraperitoneally with 131I-labeled thyroxine (T4*), and were studied at time intervals of 30 minutes and 4, 28, 48 and 72 hours after injection, 10 mice for each time interval. The organs of the central nervous system and the pituitary glands were chromatographed, and likewise serum from the same animal. The chromatographic studies revealed a compound with the same mobility as 131I-labeled triiodothyronine in the organs of the CNS and in the pituitary gland, but this compound was not present in the serum. In most of the chromatographic studies, the peaks for I, T4 and T3 coincided with those for the standards. In several instances, however, such an exact coincidence was lacking. A tentative explanation for the presence of T3* in the pituitary gland following the injection of T4* is a deiodinating system in the pituitary gland or else the capacity of the pituitary gland to concentrate T3* formed in other organs. The presence of T3* is apparently a characteristic of most of the CNS (brain, midbrain, medulla and spinal cord); but in the case of the optic nerve, the compound is not present under the conditions of this study.


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