The Persistence and Possible Externalization of Axonal Debris During Wallerian Degeneration

Schlaepfer, William W.; Hasler, Mary

doi:10.1097/00005072-197905000-00005

Cited by 22 publications

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“…In control mice, on the other hand, neurofilament degradation and the disappearance of the CAP appear to be simultaneous and very difficult to dissociate due to the rapidity of Wallerian degeneration. Previous work by Schlaepfer and colleagues (Schlaepfer, 1974(Schlaepfer, , 1977Schlaepfer and Micko, 1978;Schlaepfer and Hasler, 1979;Schlaepfer and Zimmerman, 1984; has shown that axonal and, in particular, neurofilament degradation is dependent on calcium ions. Schlaepfer and Zinlmerman (1984) also noted that the destruction of the axonal cytoskeleton, specifically the neurofilaments, is directly associated with the collapse and fragmentation of the surrounding myelin sheath.…”

Section: (In Vivo) (In Vivo) (In Virro) (In Vivo)mentioning

confidence: 99%

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Loss of the Compound Action Potential: an Electrophysiological, Biochemical and Morphological Study of Early Events in Axonal Degeneration in the C57BL/Ola Mouse

Tsao

Brown

Carden

et al. 1994

Eur J of Neuroscience

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In the C57BL/Ola (Ola) mouse strain there is a marked slowing of axonal disintegration during Wallerian degeneration. The locus of the mutation controlling this phenomenon (slow Wallerian degeneration--Wlds) has been mapped to chromosome 4, and its protective effect decreases with advancing age. Using biochemical, electrophysiological and histological techniques, the present study was undertaken to determine whether neurofilament phosphorylation and stability are altered or whether calcium-activated proteases are absent in the sciatic nerves of Ola mice. A compound action potential was detectable only when neurofilaments were present and normal axonal architecture was seen. In 1-month-old Ola mice, compound action potentials and neurofilaments were still detectable at 21 days post-transection, whereas both were undetectable by 2 days in BALB/c and C57BL/6J (6J) mice of the same age. Neurofilament levels declined faster with advancing Ola age, confirming previous results, whereas degeneration slowed in ageing BALB/c and 6J mice. In vitro and in vivo degeneration rates were comparable in BALB/c and 6J nerves. Ola nerves, however, showed more rapid decline in vitro than in vivo. Ola and BALB/c nerves frozen and then thawed and incubated in the presence of calcium ions and the ionophore A23187 were not resistant to degradation by intrinsic proteases. Even when a compound action potential could no longer be elicited, however, a majority of nerves still had > 50% of myelinated and unmyelinated axons whose electron microscopic profiles appeared normal. Thus, it appears that the first event in Wallerian degeneration in the Ola mouse is a change at the plasma membrane--a transected nerve becomes unable to conduct a compound action potential.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: (In Vivo) (In Vivo) (In Virro) (In Vivo)mentioning

confidence: 99%

“…, 1976), during which time the axons disintegrate. Observations on neurofilaments during Wallerian degeneration indicate that neurofilament immunoreactivity decreases concomitantly (Schlaepfer and Micko, 1978;Schlaepfer and Hasler, 1979;Schlaepfer and Zimmerman, 1984;Schlaepfer e t a l . , 1984).…”

Section: Introductionmentioning

confidence: 99%

Loss of the Compound Action Potential: an Electrophysiological, Biochemical and Morphological Study of Early Events in Axonal Degeneration in the C57BL/Ola Mouse

Tsao

Brown

Carden

et al. 1994

Eur J of Neuroscience

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“…Indeed, later events such as Wallerian degeneration and demyelination might be responsible for the irreversible functional loss after decompression. 4,7,[26][27][28] Such phenomena should be further investigated in future studies that link mechanical trauma to secondary cascades in compressive SCI.…”

Section: Limitations Of the Current Modelmentioning

confidence: 99%

Critical roles of decompression in functional recovery of ex vivo spinal cord white matter

Ouyang

Galle

et al. 2009

SPI

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Object The correlations between functional deficits, the magnitude of compression, and the role of sustained compression during traumatic spinal cord injury remain largely unknown. Thus, the functional outcome of this type of injury with or without surgical intervention is rather unpredictable. To elucidate how severity and duration of compression affect cord function, the authors have developed a method to study electrophysiological characteristics and axonal membrane damage in white matter from guinea pig spinal cord. Methods Ventral white matter strips isolated from adult guinea pigs were compressed by a compression rod at a level of either 60 or 80% and held briefly, for 30 minutes, or for 60 minutes. In half the experimental groups, a decompression phase consisting of probe withdrawal and 30 minutes of recovery was also applied. For all cord samples, functional response was continuously monitored through compound action potential (CAP) recording. In addition, axonal membrane damage was assessed by a horseradish peroxidase (HRP) exclusion assay. Results After 30 minutes of sustained compression at levels of 60 or 80%, a spinal cord decompression procedure caused a significant CAP recovery, with specimens reaching 97.5 ± 6.84% (p < 0.05) and 56.2 ± 6.14% (p < 0.05) of preinjury amplitude, respectively. After 60 minutes of compression, the amount of CAP recovery following the decompression stage was only 65.5 ± 9.33% for 60% compression (p < 0.05) and 29.8 ± 6.31% for 80% compression (p < 0.05). Unlike the CAP response, HRP uptake did not increase during sustained compression, and the data showed that HRP staining was primarily time dependent. Conclusions The degree of axonal membrane damage is not exacerbated during sustained compression. However, the electrical conductivity of the cord white matter weakens throughout the duration of compression. Therefore, decompression is a viable procedure for preservation of neurological function following compressive injury.

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“…Trojanowski JQ, Lee VM-Y, Schlaepfer WW: Neurofilament breakdown products in degenerating rat and human peripheral nerves. Ann Neurol 16:349-355, 1984 The factors that determine the response of neurons to axonal injury remain undefined {l, 2, 8, [21][22][23]. Axonal regeneration may be initiated by the retrograde transport of trophic factors or metabolites from the periphery Ell, 123.…”

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confidence: 99%

Neurofilament breakdown products in degenerating rat and human peripheral nerves

Trojanowski

Lee

Schalaepfer

1984

Annals of Neurology

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The fate of neurofilament (NF) proteins was examined in sections of nerves from rats that survived for 3 to 90 days following nerve transection, using anti-NF monoclonal antibodies and immunohistochemical techniques. The same methods were also applied to twenty-three human nerve biopsy specimens. Granular debris with NF immunoreactivity was observed in the rat nerves for up to 21 days after transection. Similar granular debris with NF protein immunoreactivity was observed in nerve biopsy specimens from patients with axonal degeneration. This change was most evident in specimens that demonstrated abundant ovoids in teased fiber preparations and in a patient with a recent traumatic nerve transection. Similar granular debris was not observed in normal rat or human nerves. We conclude that degenerating NF proteins have a distinctive granular appearance and that NF immunoreactivity can be demonstrated in NF breakdown products with immunohistochemical techniques for prolonged periods of time in rat and human nerves undergoing axonal degeneration. Immunohistochemical studies with anti-NF monoclonal antibodies offer a novel approach to the evaluation of human nerve biopsy specimens.

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The Persistence and Possible Externalization of Axonal Debris During Wallerian Degeneration

Cited by 22 publications

References 0 publications

Loss of the Compound Action Potential: an Electrophysiological, Biochemical and Morphological Study of Early Events in Axonal Degeneration in the C57BL/Ola Mouse

Loss of the Compound Action Potential: an Electrophysiological, Biochemical and Morphological Study of Early Events in Axonal Degeneration in the C57BL/Ola Mouse

Critical roles of decompression in functional recovery of ex vivo spinal cord white matter

Neurofilament breakdown products in degenerating rat and human peripheral nerves

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