About: Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system

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About: Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system
Creator	Dusart, I Marty, S Peschanski~, M
Source	Elsevier; Medline; PMC
abstract	Abstract Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by in situ injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei. Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes. These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time. Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.
has issue date	1992-11-30(xsd:dateTime)
bibo:doi	10.1016/0306-4522(92)90478-k
bibo:pmid	1465177
has license	els-covid
sha1sum (hex)	4462c1c009f0ac169dfa3d34817190c78ceb19c6
schema:url	https://doi.org/10.1016/0306-4522%2892%2990478-k
resource representing a document's title	Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system
has PubMed Central identifier	PMC7131789
has PubMed identifier	1465177
schema:publication	Neuroscience
resource representing a document's body	covid:4462c1c009f0ac169dfa3d34817190c78ceb19c6#body_text
is schema:about of	named entity 'excitotoxic' named entity 'CONCLUSION' named entity 'PASSAGE' named entity 'AXONS' named entity 'THEIR' named entity 'THOUGHT' named entity 'GLIAL' named entity 'SPARING' named entity 'DEMONSTRATION' named entity 'SUBMITTED' named entity 'NEURONS' named entity 'TIME' named entity 'VALIDITY' named entity 'EXCITOTOXINS' named entity 'AFFERENT' named entity 'RECENTLY' named entity 'REMYELINATION' named entity 'INDUCED' named entity 'INTERACTIONS' named entity 'LESION' named entity 'KAINATE' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'NEURONAL' named entity 'DEPLETION' named entity 'SCHWANN CELLS' named entity 'OLIGODENDROCYTES' named entity 'DEMYELINATION' named entity 'CLASSICAL' named entity 'ALTERATION' named entity 'AXONAL' named entity 'ENVIRONMENT' named entity 'KILL' named entity 'ADDITION' named entity 'PROFOUND' named entity 'WORK' named entity 'DEMYELINATION' named entity 'FIBERS' named entity 'lesion' named entity 'demonstration' named entity 'SCHWANN' named entity 'Excitotoxins' named entity 'excitotoxic' named entity 'axons' named entity 'KAINATE' named entity 'DEMYELINATION' named entity 'microglia' named entity 'axons' named entity 'myelinated' named entity 'microglia' named entity 'fine structure' named entity 'glial' named entity 'dorsal column nuclei' named entity 'oligodendrocytes' named entity 'Axonal' named entity 'Wallerian degeneration' named entity 'myelin' named entity 'complement factors' named entity 'excitotoxic' named entity 'diencephalon' named entity 'excitotoxins' named entity 'axoplasm' named entity 'astrocytes' named entity 'demyelinated' named entity 'sodium nitroprusside' named entity 'microglia' named entity 'axons' named entity 'lesion' named entity 'kainate' named entity 'axons' named entity 'Astrocytes' named entity 'glia limitans' named entity 'Schwann' named entity 'arteries' named entity 'Wallerian degeneration' named entity 'statistically significant' named entity 'kainate' named entity 'basal lamina' named entity 'axons' named entity 'neuropile'

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