THE RELATIONSHIP BETWEEN SCHMIDT‐LANTERMANN INCISURES AND MYELIN SEGMENTATION DURING WALLERIAN DEGENERATION<sup>*</sup>

Webster, Henry deF.

doi:10.1111/j.1749-6632.1965.tb20189.x

Cited by 55 publications

(15 citation statements)

References 6 publications

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“…Because developing myelin ovoids are delimited by the SLI, SLI has long been suggested to be the cleavage site of the myelin sheath (Webster, 1965; Ghabriel et al, 1979b). Studies have revealed that myelin sheath cleavage occurs adjacent to incisures rather than within SLI itself.…”

Section: Resultsmentioning

confidence: 99%

“…Demyelination in Schwann cells starts mechanically with fragmentation of the myelin sheath into small ovoid-like structures and molecularly with the down-regulation of myelin gene expression (Ghabriel and Allt, 1979a,b; Jessen and Mirsky, 2008). Morphologically, the fragmentation of myelin first occurs near SLI, including its disruption, such that the myelin ovoids are delimited by the previous locations of the SLI (Webster, 1965; Ghabriel et al, 1979b). Although authors have long observed this morphological change during demyelination, the molecular mechanisms of myelin fragmentation at SLI are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

Jung¹,

Cai²,

Lee³

et al. 2011

J. Neurosci.

127

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The mechanisms that trigger Wallerian degeneration (WD) of peripheral nerves after injury are not well understood. During the early period of WD, fragmentation of myelin into ovoid structures occurs near the Schmidt-Lantermann incisures (SLI), a noncompact region of the myelin sheath containing autotypical adherens junction. In this study, we found that new filamentous actin polymerization occurs in the SLI of mouse sciatic nerves after injury and that its inhibition prevented not only the degradation of E-cadherin in the SLI but also myelin ovoid formation. However, the inhibition of actin polymerization could not block Schwann cell dedifferentiation. The activation of Rac GTPase was observed in the distal stump of the injured nerves, and a specific Rac inhibitor, a dominant-negative Rac, and Rac1-RNA interference blocked myelin ovoid formation. Together, these findings suggest that dynamic changes in actin in the SLI are essential for initiation of demyelination after peripheral nerve injury.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

Jung¹,

Cai²,

Lee³

et al. 2011

J. Neurosci.

127

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“…The early SC responses to nerve injury are represented by morphological changes of noncompact regions such as paranodal retraction and the dilatation of SLI, long before the appearance of obvious axonal degeneration (Causey & Palmer, 1953;Ghabriel & Allt, 1979;Webster, 1965;Williams & Hall, 1971). Here, we first review how the SC contributes to remove the myelin sheath in WD.…”

Section: Early Demyelination Processes In Wallerian Degenerationmentioning

confidence: 99%

The conceptual introduction of the “demyelinating Schwann cell” in peripheral demyelinating neuropathies

Park

Kim

Tricaud

2018

Glia

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Myelinating Schwann cells undergo irreversible demyelination in many demyelinating neuropathies that show complete demyelination of the internode. Dedifferentiation, reprogramming, and myelin clearance processes—which are specifically discussed in this article—appear to be shared by various demyelinating peripheral conditions, such as Wallerian degeneration, immune‐mediated, and toxic demyelinating diseases. We propose to introduce the concept of the “demyelinating Schwann cell (DSC)” as a novel cell phenotype, which has specific properties required for myelin sheath clearance. We anticipate that the introduction of the DSC concept will provide a significant advance in understanding the pathophysiological mechanisms of demyelinating peripheral neuropathies.

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“…After nerve injury, during Wallerian degeneration, demyelination of Schwann cells occurs via fragmentation of the myelin sheath into ovoid-like structures near Schmidt-Lanterman incisures (SLI) [47–49]. Lysosomal activation is increased in Schwann cells during Wallerian degeneration [50, 51].…”

Section: Lysosomal Exocytosis and Schwann Cell Demyelinationmentioning

confidence: 99%

ATP Release through Lysosomal Exocytosis from Peripheral Nerves: The Effect of Lysosomal Exocytosis on Peripheral Nerve Degeneration and Regeneration after Nerve Injury

Jung

Kwon

et al. 2014

BioMed Research International

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Studies have shown that lysosomal activation increases in Schwann cells after nerve injury. Lysosomal activation is thought to promote the engulfment of myelin debris or fragments of injured axons in Schwann cells during Wallerian degeneration. However, a recent interpretation of lysosomal activation proposes a different view of the phenomenon. During Wallerian degeneration, lysosomes become secretory vesicles and are activated for lysosomal exocytosis. The lysosomal exocytosis triggers adenosine 5′-triphosphate (ATP) release from peripheral neurons and Schwann cells during Wallerian degeneration. Exocytosis is involved in demyelination and axonal degradation, which facilitate nerve regeneration following nerve degeneration. At this time, released ATP may affect the communication between cells in peripheral nerves. In this review, our description of the relationship between lysosomal exocytosis and Wallerian degeneration has implications for the understanding of peripheral nerve degenerative diseases and peripheral neuropathies, such as Charcot-Marie-Tooth disease or Guillain-Barré syndrome.

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THE RELATIONSHIP BETWEEN SCHMIDT‐LANTERMANN INCISURES AND MYELIN SEGMENTATION DURING WALLERIAN DEGENERATION^*

Cited by 55 publications

References 6 publications

Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

The conceptual introduction of the “demyelinating Schwann cell” in peripheral demyelinating neuropathies

ATP Release through Lysosomal Exocytosis from Peripheral Nerves: The Effect of Lysosomal Exocytosis on Peripheral Nerve Degeneration and Regeneration after Nerve Injury

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THE RELATIONSHIP BETWEEN SCHMIDT‐LANTERMANN INCISURES AND MYELIN SEGMENTATION DURING WALLERIAN DEGENERATION*

Cited by 55 publications

References 6 publications

Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

The conceptual introduction of the “demyelinating Schwann cell” in peripheral demyelinating neuropathies

ATP Release through Lysosomal Exocytosis from Peripheral Nerves: The Effect of Lysosomal Exocytosis on Peripheral Nerve Degeneration and Regeneration after Nerve Injury

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THE RELATIONSHIP BETWEEN SCHMIDT‐LANTERMANN INCISURES AND MYELIN SEGMENTATION DURING WALLERIAN DEGENERATION^*