Perinodal astrocytic processes at nodes of ranvier in developing normal and glial cell deficient rat spinal cord

Abstract

This study examined, during normal development and during the development of a glial cell deficient axon population, the nature of astrocyte involvement at the central nodes of Ranvier on spinal cord axons. One condition examined was the ventral funiculus of normal 7-day-old rats. At this age, the lumbar spinal cord underwent an active phase of gliogenesis, and axons were seen in various stages of myelination. Perinodal astrocytic processes were routinely observed at nodes of axons on which myelin sheaths exceeded 8 compact lamellae. Perinodal astrocytic processes were also seen in close proximity to axolemma at most developing nodes. This study also examined the lumbar spinal cords of rats which were X-irradiated on the third postnatal day. This procedure caused a profound reduction in the astrocyte and oligodendrocyte population in 13- and 18-day-old rats, while sparing the neuronal elements. Thus, axo-glial relationships observed in this tissue are unlikely to be random occurrences. Despite the reduction in glial cells, some oligodendrocyte-myelinated axons were observed in the irradiated spinal cords. Perinodal astrocytes were seen at all oligodendrocyte-derived nodes observed in the irradiated cord and appeared to have a specific relationship to the node of Ranvier. The presence of astrocytic processes at the normal, developing node and at the nodes in glial cell deficient spinal cords suggests that astrocytes may be necessary to the function of nodal axolemma. In irradiated spinal cords, where the glial cells are markedly reduced, apposition between astrocytic and oligodendrocytic membrane at the paranode and internode was also seen and was so common that it is highly unlikely to be due to random occurrences. These observations further suggest that in addition to the presumptive role at the nodes, astrocytes may play an inductive or supportive role in the development and maintenance of central myelin.