The nervous system of a mouse mutant characterized by a carbonic anhydrase II (CA II) deficiency was examined with light and electron microscopy and with immunocytochemistry using different glial cell markers. No major morphologic abnormalities at either the cellular or subcellular level are detectable in the brains of CAII-deficient mice, even though CAII is the main isozyme of CA in the brain. The oligodendrocytes, which characteristically express high levels of CA II, do not exhibit signs of degeneration or abnormalities even in 1-year-old CA II-deficient mice. Similarly, neurons and astrocytes have a normal structure and distribution. Oligodendrocytes show a normal staining pattern and distribution for galactocerebroside (GC), 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP), and myelin basic protein (MBP). Astrocytes have a normal morphology and distribution when stained for GFAP and S100 protein. The lack of major degeneration in the brain due to a CA II deficiency suggests these mice utilize other enzymatic or physiological pathways to compensate for the enzyme absence.
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