The ontogenic development of 2′,3′-cyclic nucleotide 3′-phosphohydrolase in the corpus callosum in relation to oligodendroglial proliferation, myelination and the distribution of fat-containing glial cells

The development of CNP'ase activity in the corpus callosum of infants dying from different causes has been compared with myelin formation and oligodendroglial proliferation determined by quantitative histological methods. Cases were classified according to the distribution of neutral lipid in capillary endothelia (Class I), with some fat-containing glial cells (Class II) or extensive occurrence of fatty glia (Class III) and compared with Class 0 cases, showing no neutral lipid accumulation. For cases in Classes II and III -in which nearly all cases of cardiorespiratory insufficiency were classified -there is a deficit of oligodendroglia and myelin, although the ratio of myelin staining intensity to glial cell numbers is similar to Class 0 cases. The deficit in myelin is due almost entirely to a reduction in oligodendroglial cell numbers. CNP'ase activity is reduced to a greater extent than myelin and the ratio of CNP'ase to glial cell number is reduced before myelination commences. The defect in expression of CNP'ase activity may be indicative of abnormal glioblast transformation. Fatty glial cells are also acquired before myelination suggesting that the primary insult to oligodendroglia, which may be hypoxia, occurs at the time of their proliferation and differentiation. Nearly half the cases of unexplained death in infancy show deficits in CNP'ase activity, correlating with reduced cell numbers and myelin, and the occurrence of fatty glial cells, all of which could be caused by hypoxia around birth.