The role of Schmidt-Lanterman incisures in Wallerian degeneration

Ghabriel, M. N.; Allt, G.

doi:10.1007/bf00691150

Cited by 37 publications

(31 citation statements)

References 9 publications

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“…3C). These observations are consistent with previously reported temporal changes in Schwann cell morphology following a peripheral nerve crush (Williams and Hall, 1971; Ghabriel and Allt;1979).…”

Section: Transduction Of Schwann Cells With Ad-lacz In Crushed Sciatisupporting

confidence: 93%

“…Previous reports have shown that injections into the sciatic nerve can easily lead to demyelination in the area of injection (Saida et al, 1978;Shy et al, 1995). Similar morphologic changes in Schwann cells have also been observed in association with the demyelination process that occurs following nerve damage, when the regular and longitudinal myelin sheaths gradually condense to more ovoid forms (Williams and Hall, 1971, Ghabriel and Allt;1979). To determine whether the observed changes in Schwann cell morphology in our experiments were due to the injection procedure itself, or whether they represented a Schwann cell response to the infection with an adenoviral vector, sciatic nerves were injected either with buffer containing 8 X 107 PFU Ad-LacZ or with buffer alone.…”

Section: Nervesmentioning

confidence: 76%

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Adenoviral Vector-Mediated Gene Delivery to Injured Rat Peripheral Nerve

Dijkhuizen

Pasterkamp

Hermens

et al. 1998

Journal of Neurotrauma

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Although much progress has been made, current treatments of peripheral nerve damage mostly result in only partial recovery. Local production of neurite outgrowth-promoting molecules, such as neurotrophins and/or cell adhesion molecules, at the site of damage may be used as a new means to promote the regeneration process. We have now explored the ability of an adenoviral vector encoding the reporter gene LacZ (Ad-LacZ) to direct the expression of a foreign gene to Schwann cells of intact and crushed rat sciatic nerves. Infusion of 8 x 10(7) PFU Ad-LacZ in the intact sciatic nerve resulted in the transduction of many Schwann cells with high levels of transgene expression lasting at least up to 12 days following viral vector administration. The efficacy of adenoviral vector delivery to a crushed nerve was investigated using three strategies. Injection of the adenoviral vector at the time of, or immediately after, a crush resulted in the transduction of only a few Schwann cells. Administration of the adenoviral vector the day after the crush resulted in the transduction of a similar number of Schwann cells 5 days after administration, as observed in uncrushed nerves. Regenerating nerve fibers were closely associated with beta-galactosidase-positive Schwann cells, indicating that the capacity of transduced Schwann cells to guide regenerating fibers was not altered. These results imply that the expression of growth-promoting proteins through adenoviral vector-mediated gene transfer may be a realistic option to promote peripheral nerve regeneration.

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Section: Transduction Of Schwann Cells With Ad-lacz In Crushed Sciatisupporting

confidence: 93%

Section: Nervesmentioning

confidence: 76%

Adenoviral Vector-Mediated Gene Delivery to Injured Rat Peripheral Nerve

Dijkhuizen

Pasterkamp

Hermens

et al. 1998

Journal of Neurotrauma

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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%

“…3A), suggesting that Rac1 may be further recruited into SLI after injury. It is plausible that the widening of SLI following nerve injury (Ghabriel and Allt, 1979a) may be related to the increased localization of Rac1 to the SLI. To determine the role of Rac1 in myelin ovoid formation in vitro , we examined the effect of a specific Rac inhibitor NSC23766 (100 μM, Nodari et al, 2007).…”

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.

129

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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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F‐actin distribution at nodes of Ranvier and Schmidt‐Lanterman incisures in mammalian sciatic nerves

et al. 2012

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Very little is known about the function of the F-actin cytoskeleton in the regeneration and pathology of peripheral nerve fibers. The actin cytoskeleton has been associated with maintenance of tissue structure, transmission of traction and contraction forces, and an involvement in cell motility. Therefore, the state of the actin cytoskeleton strongly influences the mechanical properties of cells and intracellular transport therein. In this work, we analyze the distribution of F-actin at Schmidt-Lanterman Incisures (SLI) and nodes of Ranvier (NR) domains in normal, regenerating and pathologic Trembler J (TrJ/+) sciatic nerve fibers, of rats and mice. F-actin was quantified and it was found increased in TrJ/+, both in SLI and NR. However, SLI and NR of regenerating rat sciatic nerve did not show significant differences in F-actin, as compared with normal nerves. Cytochalasin-D and Latrunculin-A were used to disrupt the F-actin network in normal and regenerating rat sciatic nerve fibers. Both drugs disrupt F-actin, but in different ways. Cytochalasin-D did not disrupt Schwann cell (SC) F-actin at the NR. Latrunculin-A did not disrupt F-actin at the boundary region between SC and axon at the NR domain. We surmise that the rearrangement of F-actin in neurological disorders, as presented here, is an important feature of TrJ/+ pathology as a Charcot-Marie-Tooth (CMT) model.

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The role of Schmidt-Lanterman incisures in Wallerian degeneration

Cited by 37 publications

References 9 publications

Adenoviral Vector-Mediated Gene Delivery to Injured Rat Peripheral Nerve

Adenoviral Vector-Mediated Gene Delivery to Injured Rat Peripheral Nerve

Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration

F‐actin distribution at nodes of Ranvier and Schmidt‐Lanterman incisures in mammalian sciatic nerves

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