Remodelling During Remyelination in the Peripheral Nervous System

Bonnaud-Toulze, Evelyne N.; Raine, Cedric S.

doi:10.1111/j.1365-2990.1980.tb00212.x

Cited by 32 publications

(15 citation statements)

References 13 publications

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“…These cells were never positive for MAG but were brightly labeled with anti-S100. Similar Schwann cell bodies have been described during recovery from experimental allergic encephalomyelitis (Bonnaud-Toulze and Raine, 1980).…”

Section: Relationship Between Sodium Channel Clustering and Mag Expresupporting

confidence: 49%

The Clustering of Axonal Sodium Channels during Development of the Peripheral Nervous System

et al. 1996

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The distribution of Na ϩ channels in rat peripheral nerve was measured during development by using immunofluorescence. Small segments of sciatic nerve from postnatal day 0 -13 (P0 -P13) pups were labeled with an antibody raised against a well conserved region of the vertebrate Na ϩ channel. At day P0 axons contained almost no Na ϩ channel aggregates. The number of clusters increased dramatically throughout the first week. In almost all cases Na ϩ channels clustered in the vicinity of Schwann cell processes. At least four classes of aggregates were noted. Clusters formed singly at Schwann cell edges, in pairs or in broad regions between neighboring Schwann cells, and in more focal zones at presumptive nodes. Almost all Na ϩ channel aggregates had reached the latter stage by the end of the first week. Histograms plotting the frequency of occurrence of each cluster type suggested a sequence of events in node formation involving the initiation of channel aggregation by Schwann cell processes. The requirement for Schwann cells during sodium channel clustering was tested by blocking proliferation of these cells with the antimitotic agent mitomycin C. Na ϩ channel clustering was sharply reduced, whereas node formation was normal at a distal site along the same nerve. Immunocytochemical detection of myelin-associated glycoprotein (MAG) indicated that Schwann cells must begin to ensheathe axons before inducing Na ϩ channel clustering.

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Section: Relationship Between Sodium Channel Clustering and Mag Expresupporting

confidence: 49%

The Clustering of Axonal Sodium Channels during Development of the Peripheral Nervous System

et al. 1996

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“…We found that ankyrin G , spectrin ␤IV, NF186, and KCNQ2 behave similarly and that specialized (ezrin-positive) Schwann cell processes remain associated with each heminode. Thus, these data provide further evidence that normal nodes consist of two heminodes that fuse during development (Dugandzija-Novakovic et al, 1995;Novakovic et al, 1996;Rasband et al, 1998;Ching et al, 1999), and there is evidence that heminodes formed under pathological conditions may rejoin to form nodes (Allt, 1969;Hall, 1973;Bonnaud-Toulze and Raine, 1980).…”

Section: Molecular Reorganization Accompanying Paranodal Demyelinationmentioning

confidence: 74%

“…It remains to be determined whether paranodal demyelination contributes to the conduction block caused by lysolecithin injections (Smith and Hall, 1980). Paranodal demyelination is also caused by wide variety of immune (Ballin and Thomas, 1969a,b;Allt, 1975;Bonnaud-Toulze and Raine, 1980), toxic (Allt, 1969;Jones and Cavanagh, 1983;Griffin et al, 1987), and mechanical (Lubinska, 1958;Ochoa, 1972;Foster et al, 1980;Dyck et al, 1990;Abe et al, 2002) agents. In spite of its potential importance, its only molecular attribute is that paranodal demyelination splits nodes into two heminodes of Na V channels (Dugandzija-Novakovic et al, 1995;Novakovic et al, 1996).…”

Section: Molecular Reorganization Accompanying Paranodal Demyelinationmentioning

confidence: 97%

Acute demyelination disrupts the molecular organization of peripheral nervous system nodes

Arroyo

Sirkowski

Chitale

et al. 2004

J of Comparative Neurology

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Intraneurally injected lysolecithin causes both segmental and paranodal demyelination. In demyelinated internodes, axonal components of nodes fragment and disappear, glial and axonal paranodal and juxtaparanodal proteins no longer cluster, and axonal Kv1.1/Kv1.2 K+ channels move from the juxtaparanodal region to appose the remaining heminodes. In paranodal demyelination, a gap separates two distinct heminodes, each of which contains the molecular components of normal nodes; paranodal and juxtaparanodal proteins are properly localized. As in normal nodes, widened nodal regions contain little or no band 4.1B. Lysolecithin also causes "unwinding" of paranodes: The spiral of Schwann cell membrane moves away from the paranodes, but the glial and axonal components of septate-like junctions remain colocalized. Thus, acute demyelination has distinct effects on the molecular organization of the nodal, paranodal, and juxtaparanodal region, reflecting altered axon-Schwann cell interactions.

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“…Several workers have described their occurrence during remyelination of the P.N.S. following experimental demyelination (Halt, 1973;King et aI., 1975;Bonnaud-Toulze &Raine, 1980), andHall (1973) suggested that these 'pseudonodes', as she termed them, developed into Schmidt-Lanterman incisures. No evidence of such transformation was found in the pups but their frequency was too low to allow definite conclusions on this point.…”

Section: Discussionmentioning

confidence: 96%

Shaking pups: a disorder of central myelination in the spaniel dog. II. Ultrastructural observations on the white matter of the cervical spinal cord

1981

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The ultrastructure of the cervical cord is described in a new canine mutant with severe hypomyelination of the C.N.S. Axons were either non-myelinated or surrounded by a myelin sheath that was markedly reduced in both its thickness and length of internode. Myelinated and non-myelinated zones were present on a single axon. There was no paucity of oligodendrocytes but many of those present contained empty or granular vacuoles within the cytoplasm. Features suggesting immaturity of myelination were commonly found at paranodes and along the internode. Abnormal inter-relationships of oligodendrocytes and astrocytes were present at many paranodes. These observations suggest an intrinsic defect of oligodendrocyte metabolism such that they are incapable of normal extension of their plasma membranes, while the cytoplasmic vacuoles may represent breakdown of defective lipids.

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Remodelling During Remyelination in the Peripheral Nervous System

Cited by 32 publications

References 13 publications

The Clustering of Axonal Sodium Channels during Development of the Peripheral Nervous System

The Clustering of Axonal Sodium Channels during Development of the Peripheral Nervous System

Acute demyelination disrupts the molecular organization of peripheral nervous system nodes

Shaking pups: a disorder of central myelination in the spaniel dog. II. Ultrastructural observations on the white matter of the cervical spinal cord

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