Protein changes during anterograde-to-retrograde conversion of axonally transported vesicles

Martz, D. C.; Garner, Judy A.; Lasek, Raymond J.

doi:10.1016/0006-8993(89)91559-x

Cited by 23 publications

(4 citation statements)

References 14 publications

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“…In the current study, progressive linear and radial expansion of the swelling occurred between 15m and 3–6h post-injury, after which swelling size was stable. This likely reflects either an interruption of further anterograde axonal transport or a conversion of anterograde to retrograde axonal transport from the swelling [41, 61, 72, 73, 7], consistent with early reorganization and recovery of the proximal axonal segment previously reported [20]. …”

Section: Discussionsupporting

confidence: 72%

Mild traumatic brain injury in the mouse induces axotomy primarily within the axon initial segment

et al. 2013

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Traumatic axonal injury (TAI) is a consistent component of traumatic brain injury (TBI), and is associated with much of its morbidity. Increasingly it has also been recognized as a major pathology of mild TBI (mTBI). In terms of its pathogenesis, numerous studies have investigated the susceptibility of the nodes of Ranvier, the paranode and internodal regions to TAI. The nodes of Ranvier, with their unique composition and concentration of ion channels, have been suggested as the primary site of injury, initiating a cascade of abnormalities in the related paranodal and internodal domains that lead to local axonal swellings and detachment. No investigation, however, has determined the effect of TAI upon the axon initial segment (AIS), a segment critical to regulating polarity and excitability. The current study sought to identify the susceptibility of these different axon domains to TAI within the neocortex, where each axonal domain could be simultaneously assessed. Utilizing a mouse model of mTBI, a temporal and spatial heterogeneity of axonal injury was found within the neocortical gray matter. Although axonal swellings were found in all domains along myelinated neocortical axons, the majority of TAI occurred within the AIS, which progressed without overt structural disruption of the AIS itself. The finding of primary AIS involvement has important implications regarding neuronal polarity and the fate of axotomized processes, while also raising therapeutic implications, as the mechanisms underlying such axonal injury in the AIS may be distinct from those described for nodal/paranodal injury.

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Section: Discussionsupporting

confidence: 72%

Mild traumatic brain injury in the mouse induces axotomy primarily within the axon initial segment

et al. 2013

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“…Parallel ultrastructural studies substantiated this finding and suggested that the dieback of the axonal swelling and its formation of the truncated appendage were not related to overt degeneration, but rather some form of axonal reorganization. In fact, this dynamic reorganization appeared consistent with the conversion of anterograde to retrograde axonal transport, which has been suggested in other experimental studies (Martz et al, 1989;Sahenk and Lasek, 1988).…”

Section: Traumatic Axonal Injury In the Optic Nervesupporting

confidence: 78%

Traumatic Axonal Injury in the Optic Nerve: Evidence for Axonal Swelling, Disconnection, Dieback, and Reorganization

Wang

Hamm

Povlishock

2011

Journal of Neurotrauma

112

146

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Traumatic axonal injury (TAI) is a major feature of traumatic brain injury (TBI) and is associated with much of its morbidity. To date, significant insight has been gained into the initiating pathogenesis of TAI. However, the nature of TAI within the injured brain precludes the consistent evaluation of its specific anterograde and retrograde sequelae. To overcome this limitation, we used the relatively organized optic nerve in a central fluid percussion injury (cFPI) model. To improve the visualization of TAI, we utilized mice expressing yellow fluorescent protein (YFP) in their visual pathways. Through this approach, we consistently generated TAI in the optic nerve and qualitatively and quantitatively evaluated its progression over a 48-h period in YFP axons via confocal microscopy and electron microscopy. In this model, delayed axonal swelling with subsequent disconnection were the norm, together with the fact that once disconnected, both the proximal and distal axonal segments revealed significant dieback, with the proximal swellings showing regression and reorganization, while the distal swellings persisted, although showing signs of impending degeneration. When antibodies targeting the C-terminus of amyloid precursor protein (APP), a routine marker of TAI were employed, they mapped exclusively to the proximal axonal segments without distal targeting, regardless of the survival time. Concomitant with this evolving axonal pathology, focal YFP fluorescence quenching occurred and mapped precisely to immunoreactive loci positive for Texas-Red-conjugated-IgG, indicating that blood-brain barrier disruption and its attendant edema contributed to this phenomenon. This was confirmed through the use of antibodies targeting endogenous YFP, which demonstrated the retention of intact immunoreactive axons despite YFP fluorescence quenching. Collectively, the results of this study within the injured optic nerve provide unprecedented insight into the evolving pathobiology associated with TAI.

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“…One of the difficulties of approaching these questions with biochemical methods is due to the large territorial dispersion of the nerve terminals of the peripheral nerves generally used in studies of axonal transport, such as sciatic nerve, for instance. However, an artificial reconcentration of a large amount of axon tips, which may keep or reestab-lish some of the mechanisms present in the nerve endings, can be obtained by crushing, ligating, or cutting the nerve (Sahenk and Lasek, 1988;Martz et al, 1989). After such lesions, most of the macromolecules that were carried in the anterograde direction accumulate at the site of injury, but a fraction of them return toward the cell body (Bray et al, 1971;Abe et al, 1974;Bisby and Bulger, 1977;Bulger and Bisby, 1978;Schmidt et al, 1980;Bisby, 1981).…”

mentioning

confidence: 99%

“…After such lesions, most of the macromolecules that were carried in the anterograde direction accumulate at the site of injury, but a fraction of them return toward the cell body (Bray et al, 1971;Abe et al, 1974;Bisby and Bulger, 1977;Bulger and Bisby, 1978;Schmidt et al, 1980;Bisby, 1981). It can be hypothesized reasonably that the reversai of these macromolecules is accomplished by a process similar to the anterograderetrograde conversion mechanism (Martz et al, 1989).…”

mentioning

confidence: 99%

Axonal Transport Reversal of Acetylcholinesterase Molecular Forms in Transected Nerve

Hässig

Tavitian

Pappalardo

et al. 1991

Journal of Neurochemistry

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Reversal of anterograde rapid axonal transport of four molecular forms of acetylcholinesterase (AChE) was studied in chick sciatic nerve during the 24-h period following a nerve transection. Reversal of AChE activity started approximately 1 h after nerve transection, and all the forms of the enzyme, except the monomeric ones, showed reversal of transport. The quantity of enzyme activity reversed 24 h after transection was twofold greater than that normally conveyed by retrograde transport. We observed no leakage of the enzyme at the site of the nerve transection and no reversal of AChE activity transport in the distal segment of the severed nerve, a result indicating that the material carried by retrograde axonal transport cannot be reversed by axotomy. Thus, a nerve transection induces both quantitative and qualitative changes in the retrograde axonal transport, which could serve as a signal of distal injury to the cell body. The velocity of reverse transport, measured within 6 h after transection, was found to be 213 mm/day, a value close to that of retrograde transport (200 mm/day). This suggests that the reversal taking place in severed sciatic nerve is similar to the anterograde-to-retrograde conversion process normally occurring at the nerve endings.

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Protein changes during anterograde-to-retrograde conversion of axonally transported vesicles

Cited by 23 publications

References 14 publications

Mild traumatic brain injury in the mouse induces axotomy primarily within the axon initial segment

Mild traumatic brain injury in the mouse induces axotomy primarily within the axon initial segment

Traumatic Axonal Injury in the Optic Nerve: Evidence for Axonal Swelling, Disconnection, Dieback, and Reorganization

Axonal Transport Reversal of Acetylcholinesterase Molecular Forms in Transected Nerve

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