Ultrastructural Analysis of Thalamus Damages in a Mouse Model of Osmotic-Induced Demyelination

Joanna Bouchat, Jacques Gilloteaux, Valérie Suain, Daniel Van Vlaender, Jean Pierre Brion, Charles Nicaise

Résultats de recherche: Contribution à un journal/une revueArticle

Résumé

A murine model used to investigate the osmotic demyelination syndrome (ODS) demonstrated ultrastructural damages in thalamus nuclei. Following chronic hyponatremia, significant myelinolysis was merely detected 48 h after the rapid reinstatement of normonatremia (ODS 48 h). In ODS samples, oligodendrocytes and astrocytes revealed injurious changes associated with a few cell deaths while both cell types seemed to endure a sort of survival strategy: (a) ODS 12 h oligodendrocytes displayed nucleoplasm with huge heterochromatic compaction, mitochondria hypertrophy, and most reclaimed an active NN cell aspect at ODS 48 h. (b) Astrocytes responded to the osmotic stress by overall cell shrinkage with clasmatodendrosis, these changes accompanied nucleus wrinkling, compacted and segregated nucleolus, destabilization of astrocyte-oligodendrocyte junctions, loss of typical GFAP filaments, and detection of round to oblong woolly, proteinaceous aggregates. ODS 48 h astrocytes regained an active nucleus aspect, without restituting GFAP filaments and still contained cytoplasmic proteinaceous deposits. (c) Sustaining minor shrinking defects at ODS 12 h, neurons showed slight axonal injury. At ODS 48 h, neuron cell bodies emerged again with deeply indented nucleus and, owing nucleolus translational activation, huge amounts of polysomes along with secretory-like activities. (d) In ODS, activated microglial cells got stuffed with huge lysosome bodies out of captures cell damages, leaving voids in interfascicular and sub-vascular neuropil. Following chronic hyponatremia, the murine thalamus restoration showed macroglial cells acutely turned off transcriptional and translational activities during ODS and progressively recovered activities, unless severely damaged cells underwent cell death, leading to neuropil disruption and demyelination.
langue originaleAnglais
Pages (de - à)144-162
journalNeurotoxicity Research
Volume36
Numéro de publication1
Les DOIs
étatPublié - 2019

Empreinte digitale

Demyelinating Diseases
Thalamus
Astrocytes
Oligodendroglia
Neuropil
Hyponatremia
Cell Death
Neurons
Polyribosomes
Osmotic Pressure
Lysosomes
Hypertrophy
Blood Vessels
Mitochondria

Citer ceci

Bouchat, Joanna ; Gilloteaux, Jacques ; Suain, Valérie ; Van Vlaender, Daniel ; Brion, Jean Pierre ; Nicaise, Charles. / Ultrastructural Analysis of Thalamus Damages in a Mouse Model of Osmotic-Induced Demyelination. Dans: Neurotoxicity Research. 2019 ; Vol 36, Numéro 1. p. 144-162.
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abstract = "A murine model used to investigate the osmotic demyelination syndrome (ODS) demonstrated ultrastructural damages in thalamus nuclei. Following chronic hyponatremia, significant myelinolysis was merely detected 48 h after the rapid reinstatement of normonatremia (ODS 48 h). In ODS samples, oligodendrocytes and astrocytes revealed injurious changes associated with a few cell deaths while both cell types seemed to endure a sort of survival strategy: (a) ODS 12 h oligodendrocytes displayed nucleoplasm with huge heterochromatic compaction, mitochondria hypertrophy, and most reclaimed an active NN cell aspect at ODS 48 h. (b) Astrocytes responded to the osmotic stress by overall cell shrinkage with clasmatodendrosis, these changes accompanied nucleus wrinkling, compacted and segregated nucleolus, destabilization of astrocyte-oligodendrocyte junctions, loss of typical GFAP filaments, and detection of round to oblong woolly, proteinaceous aggregates. ODS 48 h astrocytes regained an active nucleus aspect, without restituting GFAP filaments and still contained cytoplasmic proteinaceous deposits. (c) Sustaining minor shrinking defects at ODS 12 h, neurons showed slight axonal injury. At ODS 48 h, neuron cell bodies emerged again with deeply indented nucleus and, owing nucleolus translational activation, huge amounts of polysomes along with secretory-like activities. (d) In ODS, activated microglial cells got stuffed with huge lysosome bodies out of captures cell damages, leaving voids in interfascicular and sub-vascular neuropil. Following chronic hyponatremia, the murine thalamus restoration showed macroglial cells acutely turned off transcriptional and translational activities during ODS and progressively recovered activities, unless severely damaged cells underwent cell death, leading to neuropil disruption and demyelination.",
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Ultrastructural Analysis of Thalamus Damages in a Mouse Model of Osmotic-Induced Demyelination. / Bouchat, Joanna; Gilloteaux, Jacques; Suain, Valérie; Van Vlaender, Daniel; Brion, Jean Pierre; Nicaise, Charles.

Dans: Neurotoxicity Research, Vol 36, Numéro 1, 2019, p. 144-162.

Résultats de recherche: Contribution à un journal/une revueArticle

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AU - Bouchat, Joanna

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AU - Suain, Valérie

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AU - Brion, Jean Pierre

AU - Nicaise, Charles

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JO - Neurotoxicity Research

JF - Neurotoxicity Research

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