THE EFFECTS OF INTRAUTERINE GROWTH-RETARDATION ON THE DEVELOPMENT OF NEUROGLIA IN FETAL GUINEA-PIGS - AN IMMUNOHISTOCHEMICAL AND AN ULTRASTRUCTURAL-STUDY

The effects of intrauterine growth retardation on the development of myelinating oligodendrocytes and astrocytes in the brain and spinal cord of the fetal guinea pig have been examined using immunohistochemical and ultrastructural techniques. As judged by immunoreactivity for myelin basic protein, the extent of myelination in the spinal cord, cerebral cortex, corpus cellosum and cerebellum was reduced in the growth-retarded fetuses compared with controls at both 52 (n = 4) and 62 days (n = 5) of gestation. As assessed by immunoreactivity for glial fibrillary acidic protein, there were no marked differences between control and growth-retarded brains in the extent or distribution of radial glial cells or astrocytes at 52 or 62 days in the cerebellum. However, in the cerebral cortex at 62 days there was a striking proliferation of astrocytes surrounding cortical blood vessels in growth-retarded fetuses. Ultrastructural studies showed that at 52 days, myelination of the corticospinal tract had begun in the control but was virtually absent in growth-retarded fetuses. At 62 days, the total number of myelinated fibres in growth-retarded fetuses was significantly reduced by 56% (P < 0.01) compared with control fetuses; however, there was no difference between the groups in the total number of fibres in the corticospinal tract. Where fibres were myelinated the myelin sheath was disproportionately reduced relative to axon diameter. Thus, in intrauterine growth retardation there is a delay in the initiation and in the extent of myelination. This could be due to a reduction in the number of myelinating glia formed and the restricted capacity of those which do form to generate myelin. © 1990.