Oligodendrocytes from Jimpy and Normal Mature Tissue Can Be 'Activated' when Transplanted in a Newborn Environment

Lachapelle, F.; Lapie, P.; Gumpel, M.

doi:10.1159/000111654

Cited by 15 publications

(5 citation statements)

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“…However, it was later shown that adult murine oligodendrocytes can proliferate in response to trauma (Ludwin, 1984). In a more recent work, it has been demonstrated that in a transplantation setting oligodendrocytes (or their precursors) from a mature host can migrate to some extent and even contribute to myelination (Lachapelle et al, 1992). Hence, it is quite conceivable that host oligodendrocytes or resting oligodendrocyte precursors are activated by the embryonic graft tissue to invade the graft and contribute to graft myelination.…”

Section: Fig 5 Immunocytochemical Localization Of Amog432 Expressionmentioning

confidence: 99%

The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts

Isenmann

Molthagen

Brandner

et al. 1995

Glia

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Adhesion molecule on glia (AMOG) represents the beta 2-subunit of murine Na,K-ATPase. Mice carrying a targeted deletion of the AMOG/beta 2 gene exhibit tremor and limb paralysis at postnatal day (P) 15 and die 2 days after the onset of symptoms. The brains of these mice show edema and swelling of astrocytic end feet. However, the cause of death has remained unclear. To identify long-term consequences of AMOG/beta 2 deficiency, we have grafted parts of the embryonic telencephalic anlage of AMOG/beta 2-deficient mice into the caudoputamen of wild-type mice and analyzed the grafts up to 500 days after transplantation. Histological, immunocytochemical, and in situ hybridization techniques were applied to examine histoarchitecture, proliferation, differentiation, and long-term survival of grafts. AMOG/beta 2-deficient telencephalic grafts develop normally and form solid neural tissue that cannot be distinguished from control grafts by morphological features or with immunocytochemical stains for neuronal and glial markers. No signs of degeneration can be found. Expression analysis, however, revealed that no AMOG/beta 2 protein of possible host origin can be detected in AMOG/beta 2-deficient grafts. Graft-borne astrocytes express neither the AMOG/beta 1 nor the AMOG/beta 2 subunit of Na,K-ATPase as examined with immunocytochemistry and in situ hybridization. These findings indicate that AMOG/beta 2 is not necessary for long-term survival of telencephalic graft tissue.

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Section: Fig 5 Immunocytochemical Localization Of Amog432 Expressionmentioning

confidence: 99%

The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts

Isenmann

Molthagen

Brandner

et al. 1995

Glia

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“…The ability of transplanted glial cells to ensheath axons and synthesize myelin when transplanted into dysmyelinating mutants or chemically created models of demyelination has been studied extensively (1)(2)(3)(4)(5)(6). Until now the primary assay of myelin-forming grafts has of necessity been anatomical rather than functional or electrophysiological.…”

mentioning

confidence: 99%

Transplantation of glial cells enhances action potential conduction of amyelinated spinal cord axons in the myelin-deficient rat.

Utzschneider

Archer²,

Kocsis³

et al. 1994

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

134

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A central issue in transplantation research is to determine how and when transplantation of neural tissue can influence the development and function of the mammalian central nervous system. Of particular interest is whether electrophysiological function in the traumatized or diseased mammalian central nervous system can be improved by the replacement of cellular elements that are missing or damaged. Although it is known that transplantation of neural tissue can lead to functional improvement in models of neurological disease characterized by neuronal loss, less is known about results of transplantation in disorders of myelin. We report here that transplantation of glial cells into the dorsal columns of neonatal myelin-deflcient rat spinal cords leads to myelination and a 3-fold increase in conduction velocity. We also show that impulses can propagate into and out of the transplant region and that axons myelinated by transplanted cells do not have impaired frequency-response properties. These results demonstrate that myelination following central nervous system glial cell transplantation enhances action potential conduction in myelin-deficient axons, with conduction velocity approaching normal values.The ability of transplanted glial cells to ensheath axons and synthesize myelin when transplanted into dysmyelinating mutants or chemically created models of demyelination has been studied extensively (1-6). Until now the primary assay of myelin-forming grafts has of necessity been anatomical rather than functional or electrophysiological. However, the formation of myelin by transplanted cells does not in itself ensure secure impulse conduction. Impulse conduction after glial cell transplantation depends not only on myelination but on deployment of adequate numbers and types of ion channels at the newly formed nodes of Ranvier (7-9). Moreover, incomplete or patchy remyelination might be expected to lead to conduction failure due to impedance mismatch, which occurs at junctions between myelinated and nonmyelinated axon regions (10, 11); similarly, failure to form mature paranodal axoglial junctions can shunt action current and interfere with conduction (12, 13). In the present experiments, we transplanted central nervous system (CNS) myelin-forming cells into the spinal cord of the myelin-deficient (md) rat, a mutant that lacks CNS myelin, and studied conduction properties of the axons in the region of transplantation. The absence of host myelin in this system permits positive confirmation that functional changes seen after transplantation are due to the transplanted cells and not to background host myelination (2, 3). Electrophysiological studies from the md rat spinal cord have shown that while the amyelinated fibers ofthe md rat are capable of secure impulse conduction, they do so at -1/4 the conduction velocity of age-matched controls (14). We report here that myelination ofThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "adve...

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“…Apoptotic death is the fate of all growth factor-deprived immature oligodendrocytes (Barres et al, 1992) , raising the question of whether PLP is involved in a cell-specific survival mechanism. Moreover, after transplantation of jimpy cells into normal brains (shiverer is used for technical reasons), some oligodendrocytes survive for a very long time (Lachapelle et al, 1992). Both survival and differentiation of cultured jimpy oligodendrocytes can be improved by an astrocyte-condition medium (Bartlett et al, 1988).…”

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confidence: 99%

Neurological mouse mutants and the genes of myelin

Nave

1994

J of Neuroscience Research

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The prospect to create mouse mutants of virtually any cloned gene has renewed interest in the genetic analysis of mammalian brain development. A diverse group of spontaneous and engineered mouse mutants, characterized by a defect of myelin formation, has been intensively studied from the morphological to the molecular level. In this system, genetics has been successfully applied to analyze a corresponding set of membrane proteins which help to elaborate a defined structural entity, compact myelin. Shiverer, jimpy, Trembler, and protein zero (P0)-deficient mice demonstrate the overall function of myelination and have become models for human neurological diseases. They also illustrate some of the problems encountered in defining protein functions from complex mutant phenotypes.

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Oligodendrocytes from Jimpy and Normal Mature Tissue Can Be 'Activated' when Transplanted in a Newborn Environment

Cited by 15 publications

References 20 publications

The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts

The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts

Transplantation of glial cells enhances action potential conduction of amyelinated spinal cord axons in the myelin-deficient rat.

Neurological mouse mutants and the genes of myelin

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