Up‐Regulation of Carbonic Anhydrase Isozyme IV in CNS Myelin of Mice Genetically Deficient in Carbonic Anhydrase II

Luc P. Brion, Carlos Suarez, Hong Zhang, Wendy Cammer

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Abstract: Carbonic anhydrase (CA) II is the major CA isozyme in the brain, where it participates in acid‐base homeostasis, fluid transport, and myelin synthesis. The CA II deficiency [CA(II)D] mutation in the mouse results in structural changes in the glial cells in the CNS and in decreased susceptibility to seizures, but no detectable changes in myelin yield and ultrastructure. We compared the CA isozymes in brain and spinal cord fractions, as well as in purified myelin, between CA(II)D and control mice. CA(II)D resulted in a much lower total CA specific activity in all tissues examined but in higher CA IV specific activities in soluble and membrane‐associated fractions and pure myelin. Western blots of purified myelin showed a band corresponding to CA IV in CA(II)D mice. This band was weak or undetectable in myelin samples from normal mice. Immunocytochemical staining demonstrated CA IV in oligodendrocytes and myelinated tracts in normal mouse brains and stronger staining of the same structures in brains of CA(II)D mutants. We conclude that CA(II)D mutation in the mouse up‐regulates CNS CA IV. We speculate that this up‐regulation could mitigate the effect of CA(II)D on myelin formation and maintenance.

Original languageEnglish (US)
Pages (from-to)360-366
Number of pages7
JournalJournal of Neurochemistry
Issue number1
StatePublished - Jul 1994


  • Carbonic anhydrase
  • Central nervous system
  • Deficiency
  • Membrane bound
  • Mouse
  • Myelin
  • Regulation

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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