Antiserum induced myelination inhibition in vitro without complement

Dorfman, Susan H.; Fry, June M.; Silberberg, Donald H.

doi:10.1016/0006-8993(79)90921-1

Cited by 46 publications

(16 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…GalC/sGalC could act as an adhesion/receptor molecule coupled to a secondary signal system. Several previous observations support this molecular interpretation (Bansal and Pfeiffer 1989;Bansal et al 1988;Diaz et al 1978;Dorfman et al 1979;Ow-ens and Bunge 1990;Raine et al 1978;Ranscht et al 1982Ranscht et al , 1987Roberts 1986).…”

Section: Apoptosis Is Not Observed In Hypomyelinated Cns Of Cgt -/--Dmentioning

confidence: 60%

Galactosphingolipids and axono-glial interaction in myelin of the central nervous system

Bosio

Büssow

Adam

et al. 1998

Cell and Tissue Research

View full text Add to dashboard Cite

The myelin of central and peripheral nervous system of UDP-galactose-ceramide galactosyltransferase deficient mice (cgt-/-) is completely depleted of its major lipid constituents, galactocerebrosides and sulfatides. The deficiency of these glycolipids affects the biophysical properties of the myelin sheath and causes the loss of the rapid saltatory conduction velocity of myelinated axons. With the onset of myelination, null mutant cgt-/- mice develop fatal neurological defects. CNS and PNS analysis of cgt-/- mice revealed (1) hypomyelination of axons of the spinal cord and optic nerves, but no apoptosis of oligodendrocytes, (2) redundant myelin in younger mice leading to vacuolated nerve fibers in cgt-/- mice, (3) the occurrence of multiple myelinated CNS axons, and (4) severely distorted lateral loops in CNS paranodes. The loss of saltatory conduction is not associated with a randomization of voltage-gated sodium channels in the axolemma of PNS fibers. We conclude that cerebrosides (GalC) and sulfatides (sGalC) play a major role in CNS axono-glial interaction. A close axono-glial contact is not a prerequisite for the spiraling and compaction process of myelin. Axonal sodium channels remain clustered at the nodes of Ranvier independent of the change in the physical properties of myelin membrane devoid of galactosphingolipids. Increased intracellular concentrations of free ceramides do not trigger apoptosis of oligodendrocytes.

show abstract

Section: Apoptosis Is Not Observed In Hypomyelinated Cns Of Cgt -/--Dmentioning

confidence: 60%

Galactosphingolipids and axono-glial interaction in myelin of the central nervous system

Bosio

Büssow

Adam

et al. 1998

Cell and Tissue Research

View full text Add to dashboard Cite

show abstract

“…If this were the case, however, it is unlikely that the locomotor abilities would have been so equivalent (1). Further evidence comes from our previous demonstration in late embryos and hatchling chicks that direct focal stimulation of brainstem-spinal neurons, within the gigantocellular reticular formation (an identified brainstem locomotor region), elicited locomotor activity only in an animal transected prior to E13 (9,10,18 Antisera against GalC, the major oligodendrocyte sphingolipid (19), have been shown to demyelinate CNS tissue in vitro (20,21) and optic nerve (22,23) and spinal cord (24) We are uncertain whether the oligodendrocyte cell bodies survive our dysmyelination procedure. In vitro, the proposed mechanism of anti-GalC-induced demyelination involves microtubule disassembly and retraction of oligodendrocyte processes mediated by an influx ofextracellular calcium (21).…”

Section: Discussionmentioning

confidence: 99%

Suppression of the onset of myelination extends the permissive period for the functional repair of embryonic spinal cord.

Keirstead

Hasan

Muir

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

146

View full text Add to dashboard Cite

In an embryonic chicken, traneto of the thoracic spinal cord prior to embryonic day (E) The anatomical development and functional organization of avian descending brainstem-spinal pathways concerned with locomotion is similar to that of other vertebrates, including mammals (1,(5)(6)(7)(8)(9)(10). If the thoracic spinal cord of an embryonic chicken is transected prior to day 13 (E13) of the 21-day developmental period, the animal will subsequently effect complete neuroanatomical and physiological repair resulting in total functional recovery (8-10). Most importantly, regeneration of previously severed axonal fibers contributes to this repair process (10

show abstract

“…oligodendrocyte differentiation and myelination by acting as sensors/transmitters of environmental information" (Bansal et al, 1988;. This hypothesis has been supported by our findings using anti-galactolipid antibody perturbation and biochemical inhibition of sulfatide synthesis (Bansal et al, 1988;Pfeiffer, 1989, 1994a,b) (this report), as well as by a number of other observations related to the role of not only galactolipids but also gangliosides (for review, see Bansal et al, 1988;Coetzee et al, 1998;e.g., Diaz et al, 1978;Dorfman et al, 1979;Ranscht et al, 1982Ranscht et al, , 1987Dyer and Benjamins, 1988;Pettmann et al, 1988;Wu and Ledeen, 1991;Yim et al, 1994). These studies demonstrate that the interaction of these galactolipids with the environment leads to biological responses.…”

Section: Discussionmentioning

confidence: 99%

Negative Regulation of Oligodendrocyte Differentiation by Galactosphingolipids

1999

View full text Add to dashboard Cite

Galactocerebroside and sulfatide, major galactosphingolipid components of oligodendrocyte plasma membranes and myelin, are first expressed at a critical point, when progenitors cease to proliferate and commence terminal differentiation. We showed previously that an antibody to galactocerebroside/ sulfatide arrested terminal differentiation, suggesting a role for these galactolipids in oligodendrocyte differentiation. We have now investigated the differentiation of oligodendrocytes (1) in response to other anti-galactolipid antibodies, showing that anti-sulfatide O4 but not anti-galactocerebroside O1 blocks terminal differentiation, perhaps by mimicking an endogenous ligand, and (2) in a transgenic mouse unable to synthesize these lipids because of mutation of the gene for ceramide galactosyltransferase, a key enzyme for galactosphingolipid synthesis. We find that galactosyltransferase mRNA expression begins at the late progenitor [pro-oligodendroblast (Pro-OL)] stage of the lineage and that the late progenitor marker prooligodendroblast antigen is not synthesized in the absence of galactosyltransferase. The principal outcome of the elimination of these galactolipids is a two-to threefold enhancement in the number of terminally differentiated oligodendrocytes both in culture and in vivo. Because the general pattern of differentiation and the level of progenitor proliferation and survival appear to be unaltered in the mutant cultures, we conclude that the increased number of oligodendrocytes is caused by an increased rate and probability of differentiation. In agreement with these two experimental approaches, we present a model in which galactosphingolipids (in particular galactocerebroside and/or sulfatide) act as sensors and/or transmitters of environmental information, interacting with endogenous ligands to function as negative regulators of oligodendrocyte differentiation, monitoring the timely progress of Pro-OLs into terminally differentiating, myelin-producing oligodendrocytes.

show abstract

Antiserum induced myelination inhibition in vitro without complement

Cited by 46 publications

References 25 publications

Galactosphingolipids and axono-glial interaction in myelin of the central nervous system

Galactosphingolipids and axono-glial interaction in myelin of the central nervous system

Suppression of the onset of myelination extends the permissive period for the functional repair of embryonic spinal cord.

Negative Regulation of Oligodendrocyte Differentiation by Galactosphingolipids

Contact Info

Product

Resources

About