Early development and dispersal of oligodendrocyte precursors in the embryonic chick spinal cord

Development ◽  
1995 ◽  
Vol 121 (6) ◽  
pp. 1743-1754 ◽  
Author(s):  
K. Ono ◽  
R. Bansal ◽  
J. Payne ◽  
U. Rutishauser ◽  
R.H. Miller
Keyword(s):  
Spinal Cord ◽  
Ventricular Zone ◽  
General Characteristic ◽  
Central Canal ◽  
Vertebrate Development ◽  
Dorsal Spinal Cord ◽  
Oligodendrocyte Precursors ◽  
Dorsal Spinal ◽  
Chick Spinal Cord

Oligodendrocytes, the myelinating cells of the vertebrate CNS, originally develop from cells of the neuroepithelium. Recent studies suggest that spinal cord oligodendrocyte precursors are initially localized in the region of the ventral ventricular zone and subsequently disperse throughout the spinal cord. The characteristics of these early oligodendrocyte precursors and their subsequent migration has been difficult to assay directly in the rodent spinal cord due to a lack of appropriate reagents. In the developing chick spinal cord, we show that oligodendrocyte precursors can be specifically identified by labeling with O4 monoclonal antibody. In contrast to rodent oligodendrocyte precursors, which express O4 immunoreactivity only during the later stages of maturation, in the chick O4 immunoreactivity appears very early and its expression is retained through cellular maturation. In embryos older than stage 35, O4+ cells represent the most immature, self-renewing, cells of the chick spinal cord oligodendrocyte lineage. In the intact chick spinal cord, the earliest O4+ cells are located at the ventral ventricular zone where they actually contribute to the ventricular lining of the central canal. The subsequent migration of O4+ cells into the dorsal region of the spinal cord temporally correlates with the capacity of isolated dorsal spinal cord to generate oligodendrocytes in vitro. Biochemical analysis suggests O4 labels a POA-like antigen on the surface of chick spinal cord oligodendrocyte precursors. These studies provide direct evidence for the ventral ventricular origin of spinal cord oligodendrocytes, and suggest that this focal source of oligodendrocytes is a general characteristic of vertebrate development.

Sonic hedgehog signaling is required during the appearance of spinal cord oligodendrocyte precursors

Development ◽  
1999 ◽  
Vol 126 (11) ◽  
pp. 2419-2429 ◽  
Author(s):  
D.M. Orentas ◽  
J.E. Hayes ◽  
K.L. Dyer ◽  
R.H. Miller
Keyword(s):  
Spinal Cord ◽  
Sonic Hedgehog ◽  
Ventricular Zone ◽  
Developmental Period ◽  
Dorsal Spinal Cord ◽  
Shh Signaling ◽  
Oligodendrocyte Precursors ◽  
Dorsal Spinal

Spinal cord oligodendrocyte precursors arise in the ventral ventricular zone as a result of local signals. Ectopic oligodendrocyte precursors can be induced by sonic hedgehog (Shh) in explants of chick dorsal spinal cord over an extended developmental period. The role of Shh during normal oligodendrocyte development is, however, unclear. Here we demonstrate that Shh is localized to the ventral spinal cord immediately prior to, and during the appearance of oligodendrocyte precursors. Continued expression of Shh is required for the appearance of spinal cord oligodendrocyte precursors as neutralization of Shh signaling both in vivo and in vitro during a defined developmental period blocked their emergence. The inhibition of oligodendrocyte precursor emergence in the absence of Shh signaling was not the result of inhibiting precursor cell proliferation, and the neutralization of Shh signaling after the emergence of oligodendrocyte precursors had no effect on the appearance of additional cells or their subsequent differentiation. Similar concentrations of Shh induce motor neurons and oligodendrocytes in dorsal spinal cord explants. However, in explants from early embryos the motor neuron lineage is preferentially expanded while in explants from older embryos the oligodendrocyte lineage is preferentially expanded.

Oligodendrocyte precursors originate at the ventral ventricular zone dorsal to the ventral midline region in the embryonic rat spinal cord

Development ◽  
1993 ◽  
Vol 118 (2) ◽  
pp. 563-573 ◽  
Author(s):  
E. Noll ◽  
R.H. Miller
Keyword(s):  
Spinal Cord ◽  
Ventricular Zone ◽  
Rat Spinal Cord ◽  
Proliferating Cells ◽  
Dorsal Spinal Cord ◽  
Ventral Midline ◽  
Ventricular Cells ◽  
Oligodendrocyte Precursors ◽  
Dorsal Spinal ◽  
Ventral Spinal Cord

The precursors for oligodendrocytes, the myelinating cells of the vertebrate CNS, appear to be initially restricted to ventral regions of the embryonic rat spinal cord. These cells subsequently populate dorsal spinal cord regions where they acquire the mature characteristics of oligodendrocytes. To determine the location and timing of proliferation of oligodendrocyte precursors in the ventral spinal cord, and to map their pathways of migration in vivo, an assay that identifies mitotic cells was used in conjunction with antibodies that distinguish astrocytes, oligodendrocytes and their precursors. Between E16.5 and E18.5, two hours after a maternal injection of BrdU, the majority of proliferating cells were located in a discrete cluster at the ventral ventricular zone dorsal to the ventral midline region of the developing spinal cord. By contrast, 12–24 hours following a BrdU injection at E16.5, increasing numbers of labeled cells were seen in the dorsal and more lateral locations of the spinal cord. These observations suggest that BrdU-labeled ventral ventricular cells, or their progeny migrate dorsally and laterally during subsequent spinal cord development. To determine the nature of these proliferating cells, cultures of dorsal and ventral spinal cord from BrdU-labeled animals were double-labeled with antibodies that identify oligodendrocytes or astrocytes and anti-BrdU. In dorsal spinal cord cultures derived from animals that had received a single injection of BrdU at E16.5, the majority of proliferating cells differentiated into astrocytes while, in ventrally derived cultures from the same animals, the majority of proliferating cells differentiated into oligodendrocytes. In dorsal cultures prepared from animals that received multiple injections of BrdU between E16.5 and E18.5, many more cells were labeled with BrdU and approximately half of these differentiated into oligodendrocytes. These observations suggest that during embryonic development proliferating oligodendrocyte precursors are initially located at the ventral ventricular zone dorsal to the ventral midline region of the spinal cord and during subsequent maturation these cells or their progeny migrated dorsally in the ventricular region of the spinal cord, and laterally to reside in the developing white matter.

Regulation of oligodendrocyte differentiation: a role for retinoic acid in the spinal cord

Development ◽  
1994 ◽  
Vol 120 (3) ◽  
pp. 649-660
Author(s):  
E. Noll ◽  
R.H. Miller
Keyword(s):  
Spinal Cord ◽  
Retinoic Acid ◽  
Embryonic Development ◽  
Ventricular Zone ◽  
Distinct Group ◽  
Oligodendrocyte Differentiation ◽  
Distinct Cell ◽  
Embryonic Spinal Cord ◽  
Oligodendrocyte Precursors

During development, oligodendrocyte precursors undergo sequential stages of differentiation characterized by expression of distinct cell surface properties and proliferative responses. Although both PDGF and bFGF are mitogenic for these cells, the factors that regulate the progression of oligodendrocyte precursors through their differentiative program remain unclear. One factor present in the embryonic spinal cord that may regulate differentiation of oligodendrocyte precursors is retinoic acid. Here we show that retinoic acid inhibits the maturation of embryonic spinal cord oligodendrocyte precursors in vitro at an early, highly motile stage of differentiation, characterized by the expression of A2B5 immunoreactivity. Basic FGF acts both as a mitogen and an inhibitor of spinal cord oligodendrocyte precursor maturation, but at a significantly later stage of differentiation, characterized by the expression of O4 immunoreactivity. In the presence of RA both the mitogenic and differentiation inhibiting effects of bFGF are abolished, consistent with RA acting as an early regulator of oligodendrocyte differentiation. During embryonic development, oligodendrocyte precursors arise initially from a distinct group of cells at the ventral ventricular zone of the spinal cord. Myelination of the entire spinal cord is dependent on the migration of immature precursor cells to peripheral developing white matter. Since the embryonic spinal cord has the capacity to release relatively high levels of retinoids, we propose that RA inhibits oligodendrocyte differentiation during early embryonic development permitting their dispersal throughout the entire spinal cord.

Idiopathic dorsal spinal cord herniation perforating the lamina: a case report and review of the literature

2021 ◽  
Author(s):  
Haruki Funao ◽  
Satoshi Nakamura ◽  
Kenshi Daimon ◽  
Norihiro Isogai ◽  
Yutaka Sasao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Case Report ◽  
Review Of The Literature ◽  
Dorsal Spinal Cord ◽  
Spinal Cord Herniation ◽  
Dorsal Spinal

Spinal integration of antidromic mediated cutaneous vasodilation during dorsal spinal cord stimulation in the rat

1999 ◽  
Vol 260 (3) ◽  
pp. 173-176 ◽  
Author(s):  
Kirk W. Barron ◽  
John E. Croom ◽  
Crystal A. Ray ◽  
Margaret J. Chandler ◽  
Robert D. Foreman
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Stimulation ◽  
Dorsal Spinal Cord ◽  
Cutaneous Vasodilation ◽  
Dorsal Spinal

Forskolin and phosphodiesterase inhibitors release adenosine but inhibit morphine-evoked release of adenosine from spinal cord synaptosomes

1991 ◽  
Vol 69 (6) ◽  
pp. 877-885 ◽  
Author(s):  
D. Nicholson ◽  
T. D. White ◽  
J. Sawynok
Keyword(s):  
Spinal Cord ◽  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Phosphodiesterase Inhibitors ◽  
Dorsal Spinal Cord ◽  
Adenosine Release ◽  
Basal Release ◽  
Phosphodiesterase Isoenzymes ◽  
Dorsal Spinal ◽  
Ventral Spinal Cord

The effects of forskolin, Ro 20-1724, rolipram, and 3-isobutyl-1-methylxanthine (IBMX) on morphine-evoked release of adenosine from dorsal spinal cord synaptosomes were evaluated to examine the potential involvement of cyclic AMP in this action of morphine. Ro 20-1724 (1–100 μM), rolipram (1–100 μM), and forskolin (1–10 μM) increased basal release of adenosine, and at 1 μM inhibited morphine-evoked release of adenosine. Release of adenosine by Ro 20-1724, rolipram, and forskolin was reduced 42–77% in the presence of α, β-methylene ADP and GMP, which inhibits ecto-5′-nucleotidase activity by 81%, indicating that this adenosine originated predominantly as nucleotide(s). Significant amounts of adenosine also were released from the ventral spinal cord by these agents. Ro 20-1724 and rolipram did not significantly alter the uptake of adenosine into synaptosomes. Although Ro 20-1724 and rolipram had only limited effects on the extrasynaptosomal conversion of added cyclic AMP to adenosine, IBMX, a phosphodiesterase inhibitor with a broader spectrum of inhibitory activity for phosphodiesterase isoenzymes, significantly inhibited the conversion of cyclic AMP to adenosine and resulted in recovery of a substantial amount of cyclic AMP. As with the non-xanthine phosphodiesterase inhibitors, IBMX increased basal release of adenosine and reduced morphine-evoked release of adenosine. Adenosine released by IBMX was reduced 70% in the presence of α, β-methylene ADP and GMP, and release from the ventral spinal cord was 61% of that from the dorsal spinal cord. Collectively, these results indicate that forskolin and phosphodiesterase inhibitors release nucleotide(s) which is (are) converted extrasynaptosomally to adenosine. For forskolin, Ro 20-1724, and rolipram, the nucleotide released could be cyclic AMP. Morphine releases adenosine per se, and forskolin and phosphodiesterase inhibitors reduce this release. The lack of increase in the action of morphine with phosphodiesterase inhibitors in particular does not support a role for stimulation of cyclic AMP production by morphine in the release of adenosine. The reduction in morphine-evoked release of adenosine by forskolin and phosphodiesterase inhibitors suggests either (a) that a reduction in cyclic levels by morphine promotes adenosine release, or (b) that cyclic AMP interferes with the release process.Key words: forskolin, Ro 20-1724, 3-isobutyl-1-methylxanthine, cyclic AMP, morphine, adenosine release, spinal cord.

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