Astrocytes are an early target in osmotic demyelination syndrome

Fabrice Gankam Kengne, Charles Nicaise, Alain Soupart, Alain Boom, Johan Schiettecatte, Roland Pochet, Jean Pierre Brion, Guy Decaux

Research output: Contribution to journalArticlepeer-review


Abrupt osmotic changes during rapid correction of chronic hyponatremia result in demyelinative brain lesions, but the sequence of events linking rapid osmotic changes to myelin loss is not yet understood. Here, in a rat model of osmotic demyelination syndrome, we found that massive astrocyte death occurred after rapid correction of hyponatremia, delineating the regions of future myelin loss. Astrocyte death caused a disruption of the astrocyte-oligodendrocyte network, rapidly upregulated inflammatory cytokines genes, and increased serum S100B, which predicted clinical manifestations and outcome of osmotic demyelination. These results support a model for the pathophysiology of osmotic brain injury in which rapid correction of hyponatremia triggers apoptosis in astrocytes followed by a loss of trophic communication between astrocytes and oligodendrocytes, secondary inflammation, microglial activation, and finally demyelination.
Original languageEnglish
Pages (from-to)1834-45
Number of pages12
JournalJournal of the American Society of Nephrology : JASN
Issue number10
Publication statusPublished - Oct 2011


  • Animals
  • Astrocytes
  • Blood-Brain Barrier
  • Cell Death
  • Connexins
  • Demyelinating Diseases
  • Disease Models, Animal
  • Down-Regulation
  • Gene Expression Regulation
  • Hypertrophy
  • Hyponatremia
  • Lymphocytes
  • Male
  • Microglia
  • Myelin Sheath
  • Nerve Growth Factors
  • Neutrophil Infiltration
  • Osmotic Pressure
  • Rats
  • Rats, Wistar
  • S100 Calcium Binding Protein beta Subunit
  • S100 Proteins
  • Saline Solution, Hypertonic
  • Sodium


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