Evidence for the ventral origin of oligodendrocyte precursors in the rat spinal cord

Abstract

The neuroepithelial cells of the mammalian neural tube are thought to give rise to all classes of differentiated neurons and macroglial cells in the adult CNS. In most cases, the regulation and timing of commitment of neuroepithelial cells to specific differentiative pathways are unknown. It has been proposed that in developing spinal cord, the macroglial cells--astrocytes and oligodendrocytes--arise either by the direct transformation of radial glial cells in the developing cord or, alternatively, by the differentiation of distinct precursor cells which migrate to presumptive white matter from the region of the central canal during development. In this study, the timing of oligodendrocyte differentiation in different levels of the spinal cord and the capacity of specific regions of the spinal cord to give rise to oligodendrocytes at various ages was tested in vitro. At embryonic day 14, all complete segments, as well as all ventral regions along the rostral-caudal axis of the spinal cord, have the capacity for oligodendrogenesis. By contrast, dorsal regions of the thoracic and lumbar spinal cord do not develop the capacity for oligodendrogenesis until later in development. The capacity of dorsal rat spinal cord to give rise to oligodendrocytes appears to be associated with the ventral-to-dorsal migration of oligodendrocyte precursors. These observations suggest that commitment to an oligodendrocyte differentiative pathway appears to occur in a distinct population of ventrally located glial precursors in the embryonic rat spinal cord.

Spatiotemporal gradient of oligodendrocyte differentiation in chick optic tectum requires brain integrity and cell‐cell interactions

“…Therefore, the ordered appearance of these cells in vivo requires the OT to be intact. This seems to be fundamentally different from mammals, where oligodendrocytes arise in high-density (Williams et al, 1985;Warf et al, 1991) and clonal Temple and Raff, 1986) cultures with approximately the same timing as in vivo. Differentiation of OT cells here occurred without induction by extrinsic factors and therefore is more likely to be a removal of inhibitory influences that operate in the intact brain than a direct positive induction, although it is possible that removal of tissue from the intact brain triggered intrinsic induction to occur.…”

“…Spinal cord oligodendrocytes apparently arise only from ventral regions and then migrate dorsally to fill the remainder of the cord (Warf et al, 1991;Noll and Miller, 1993;Pringle and Richardson, 1993;Hall et al, 1996;Ono et al, 1997b;Miller et al, 1999;Sussman et al, 2000). In mammalian brain, oligodendrocytes have been reported to arise from the subventricular zone and migrate to both gray and white matter of the ipsilateral forebrain hemisphere (Levison and Goldman, 1993).…”

Distribution of CD9 in the developing and mature rat nervous system

“…7). In contrast, Warf et al (1991) demonstrated the ability of ventral but not dorsal spinal cord to give rise to oligodendrocytes in culture at E14.5. At later ages,both ventral and dorsal cord contain oligodendrocyte precursors, possibly due to migration of these from their ventral origin.…”

Isolation of a Novel Platelet-Derived Growth Factor-Responsive Precursor from the Embryonic Ventral Forebrain

“…Furthermore, the in vitro isolation of glial-restricted precursors (GRPs) from the spinal cord (Rao and Mayer-Proschel, 1997;Rao et al, 1998), and their transplantation and differentiation into astrocytes and oligodendrocytes (Rao and Mayer-Proschel, 1997;Rao et al, 1998;Herrera et al, 2001), supports such a lineage model. However, the fact that GRPs can be isolated from dorsal as well as ventral embryonic spinal cords contrasts with studies demonstrating the ventral restriction of OLPs (Warf et al, 1991;Pringle and Richardson, 1993;Ono et al, 1995;Lu et al, 2002;Zhou and Anderson, 2002). This may be reconciled by the findings of Gabay et al (2003), who found that the deregulation of dorsoventral patterning in vitro, attributable in part to aberrant SHH production induced by fibroblast growth factor (FGF) signaling, may be responsible for the generation of oligodendrocytes by dorsally derived GRPs.…”