Incorporation of axonally transported glycoproteins into axolemma during nerve regeneration

Griffin, JW; Price, D. G.; Drachman, D. B.; Morris, James R.

doi:10.1083/jcb.88.1.205

Cited by 109 publications

(46 citation statements)

References 36 publications

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“…Local incorporation of proteins into the axolemma, probably by means of vesicle fusion, has been suggested. 22 In a previous ultrastructural study, 64 we discovered that during axonal regeneration of the sciatic nerve in the adult rat, the proximal axolemma of unmyelinated axons was enriched in B-50/GAP-43 in comparison to the intact unmyelinated axon. In line with this finding, it could be that B-50/GAP-43 carrying vesicles locally fuse with unmyelinated axolemma and attach B-50/GAP-43 during the translocation.…”

Section: B-50/growth-associated Protein-43 May Be Transported To the mentioning

confidence: 91%

Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

et al. 1996

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Abstract--The growth-associated protein-43/B-50 (B-50/GAP-43) is conveyed from the neuronal soma into the axon by fast axonal transport and moved to the nerve terminal. To visualize and determine the type of vesicles by which B-50/GAP-43 is anterogradely transported in the regenerating rat sciatic nerve, we have investigated Lowicryl HM20 embedded nerve pieces dissected from the proximal side of a collection ligature. Ultrastructurally, numerous vesicular profiles of various sizes, tubules and mitochondria were seen to accumulate proximal to the collection ligature. Both, in unmyelinated and myelinated axons, B-50/GAP-43 immunoreactivity was associated with vesicular profiles which had a diameter of 50 nm. A fraction of the B-50/GAP-43 label co-localized with the small vesicle marker synaptophysin. Co-localization of B-50/GAP-43 was not detected with the large dense-core vesicle marker calcitonin gene-related peptide.These results indicate that, in rat sciatic nerve axons, B-50/GAP-43 is anterogradely transported in small 50 nm vesicles of the constitutive pathway. These transport vesicles were distinguished in two types. We suggest that one type carrying, both, B-50 GAP-43 and synaptophysin has as destination the nerve terminal, whereas the second type, which only contains B-50/GAP-43 and no synaptophysin, may be primarily targeted to the axolemma for local membrane fusion.

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Section: B-50/growth-associated Protein-43 May Be Transported To the mentioning

confidence: 91%

Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

et al. 1996

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“…In some fibres the presence of focal damage to the nodal axon was also reflected in the abnormalities of the axoplasm beneath the node, with swelling and local accumulation of cytoskeletal elements and/or particulate organelles. How the nodal lengthening occurs is speculative; it may involve insertion of new membrane from vesicles carried by fast axonal transport, as happens during nerve regeneration (Tessler et al, 1980;Griffin et al, 1981), or it could involve displacement of the myelin sheath attachment sites away from the node (Korobkin et al, 1975;Jones & Cavanagh, 1983;Stanley et al, 1985;Griffin et al, 1987).…”

Section: Early Changes At the Node And Paranodementioning

confidence: 98%

Early nodal changes in the acute motor axonal neuropathy pattern of the Guillain-Barré syndrome

Griffin

Macko³

et al. 1996

J Neurocytol

232

146

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The axonal patterns of Guillain-Barré syndrome, associated in many cases with antecedent Campylobacter jejuni infection, are now recognized as frequent causes of acute flaccid paralysis in some regions of the world. This study examined ultrastructurally the PNS of seven cases of the acute motor axonal neuropathy form of Guillain-Barré syndrome. In this disorder previous studies of advanced cases have found Wallerian-like degeneration of motor fibres in the spinal roots and peripheral nerves, with little lymphocytic inflammation or demyelination. The present study was focused on identifying early changes and establishing the sequence of changes. By electron microscopy the earliest and mildest changes consisted of lengthening of the node of Ranvier with distortion of the paranodal myelin, and in some instances with breakdown of the outermost myelin terminal loops. At this stage many nodes had overlying macrophages which extended their processes through the Schwann cell basal lamina covering the node and apposed the axolemma. Macrophage processes then extended beneath the myelin terminal loops, and the whole macrophage entered the periaxonal space at the paranode. Macrophage processes dissected the axon from the adaxonal Schwann cell plasmalemma and the macrophages advanced into the internodal periaxonal space, where they typically surrounded a condensed-appearing axon. At this stage the adaxonal Schwann cell cytoplasm regularly degenerated and disappeared, so that the periaxonal space was bounded by the innermost myelin lamella, and the axolemma of many fibres could not be seen. The internodal myelin sheath and the abaxonal Schwann cell cytoplasm remained normal. This arrangement appeared to be stable for some time, but in many fibres the axon subsequently underwent Wallerian-like degeneration. By interfering with impulse conduction, these nodal and periaxonal changes may explain paralysis in some pathologically mild cases. In addition, at early stages, these changes may be reversible, thus explaining the rapid recovery of some patients who become paralysed with acute motor axonal neuropathy. These observations, taken together with previous studies, suggest that acute motor axonal neuropathy is an antibody- and complement-mediated disorder in which the relevant epitopes are present on the nodal and internodal axolemma.

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“…These same blocks were used for electron microscopy employing previously described techniques (Griffin et al, 1981).…”

Section: Tissue Processingmentioning

confidence: 99%

Epidermal reinnervation after intracutaneous axotomy in man

Rajan

Polydefkis

Hauer

et al. 2003

J of Comparative Neurology

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Two distinct patterns of reinnervation occur after injury to the cutaneous nerves: regenerative growth of the injured nerve and "collateral sprouting" of neighboring intact nerves. We describe two complementary models of regrowth of transected small sensory fibers in human skin. The "incision" model uses a circular incision that transects the subepidermal plexus, resulting in Wallerian degeneration of the nerve fibers that enter the incised cylinder, leaving a defined zone of denervated dermis and epidermis. The "excision" model utilizes an identical incision, followed by removal of the incised cylinder of skin, leaving a denervated area in which Schwann cells are absent. In the incision model, the earliest reinervation of denervated epidermis occurred by collateral sprouting from the terminals of epidermal axons from just outside the incision line. These axon terminals extended horizontally across the incision line and through the superficial layers of the epidermis, beneath the stratum corneum. By 13 days, numerous regenerating axons appeared in the deeper dermis derived from transected axons. These regenerating axons grew toward and ultimately into the epidermis, so that epidermal axonal density had normalized by 30-75 days. The invasion of these axons was associated with regression of the horizontally growing collateral sprouts. In the excision model, new fibers arose by terminal elongation of the epidermal axons outside the incision line, as in the incision model, and especially by collateral branching of epidermal fibers at the incision margins. These collaterals reached the epidermal surface of the basal lamina at the dermal-epidermal junction and then grew slowly toward the center of the denervated circle. In contrast to the incision model, however, complete reinnervation was not achieved even after 23 months. These models can be used to study reinnervation of denervated skin in man in different injury models and have relevance for exploring the stimuli for axonal growth and remodeling.

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Incorporation of axonally transported glycoproteins into axolemma during nerve regeneration

Cited by 109 publications

References 36 publications

Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

Ultrastructural localization of B-50/growth-associated protein-43 to anterogradely transported synaptophysin-positive and calcitonin gene-related peptide-negative vesicles in the regenerating rat sciatic nerve

Early nodal changes in the acute motor axonal neuropathy pattern of the Guillain-Barré syndrome

Epidermal reinnervation after intracutaneous axotomy in man

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