ArticleCellular and molecular neurobiology2013
Short-term cuprizone feeding induces selective amino acid deprivation with concomitant activation of an integrated stress response in oligodendrocytes.
Article in Cellular and molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- Loss of oligodendrocyte transcription factor 2 protein expression in metabolically stressed oligodendrocytes.Acta neuropathologica · 2026Article
- GCN2-Mediated eIF2α Phosphorylation Is Required for Central Nervous System Remyelination.International journal of molecular sciences · 2025Article
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
- Article
- The Tryptophan-Kynurenine Metabolic System Is Suppressed in Cuprizone-Induced Model of Demyelination Simulating Progressive Multiple Sclerosis.Biomedicines · 2023Article
- Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity.Cardiovascular toxicology · 2023Article
- Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance.Molecular neurodegeneration · 2022Article
- Siponimod ameliorates metabolic oligodendrocyte injury via the sphingosine-1 phosphate receptor 5.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- The mechanistic target of rapamycin as a regulator of metabolic function in oligodendroglia during remyelination.Current opinion in pharmacology · 2022Review
- Article
- Nile Red fluorescence spectroscopy reports early physicochemical changes in myelin with high sensitivity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cuprizone markedly decreases kynurenic acid levels in the rodent brain tissue and plasma.Heliyon · 2021Article
- Cannabidiol Displays Proteomic Similarities to Antipsychotics in Cuprizone-Exposed Human Oligodendrocytic Cell Line MO3.13.Frontiers in molecular neuroscience · 2021Article
- Evaluation of neuroprotective effects of alpha-tocopherol in cuprizone-induced demyelination model of multiple sclerosis.Research in pharmaceutical sciences · 2020Article
- Guanabenz modulates microglia and macrophages during demyelination.Scientific reports · 2020Article
- The active contribution of OPCs to neuroinflammation is mediated by LRP1.Acta neuropathologica · 2020Article
- Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice.Histochemistry and cell biology · 2019Article
- Animal Weight Is an Important Variable for Reliable Cuprizone-Induced Demyelination.Journal of molecular neuroscience : MN · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuprizone [bis(cyclohexylidenehydrazide)]-induced toxic demyelination is an experimental approach frequently used to study de- and re-myelination in the central nervous system. In this model, mice are fed with the copper chelator cuprizone which leads to oligodendrocyte apoptosis and subsequent microgliosis, astrocytosis, and demyelination. The underlying mechanisms of cuprizone-induced oligodendrocyte death are still unknown. We analysed differences in amino acid levels after short-term cuprizone exposure (i.e., 4 days). Furthermore, an amino acid response (AAR) pathway activated in oligodendrocytes after cuprizone intoxication was evaluated. Short-term cuprizone exposure resulted in a selective decrease of alanine, glycine, and proline plasma levels, which was paralleled by an increase of apoptotic cells in the liver and a decrease of alanine aminotransferase in the serum. These parameters were paralleled by oligodendrocyte apoptosis and the induction of an AAR with increased expression of the transcription factors ATF-3 and ATF-4 (activating transcription factor-3 and -4). Immunohistochemistry revealed that ATF-3 is exclusively expressed by oligodendrocytes and localized to the nuclear compartment. Our results suggest that cuprizone-induced liver dysfunction results in amino acid starvation and in consequence to the activation of an AAR. We propose that this stress response modulates oligodendrocyte viability in the cuprizone animal model.
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