Reciprocal Schwann cell-axon interactions

Reynolds, M. L.; Woolf, Clifford J.

doi:10.1016/0959-4388(93)90139-p

Cited by 144 publications

(95 citation statements)

References 62 publications

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“…Based on our finding that sensory axon-derived neuregulin supports the survival of Schwann cells associated with developing mechanoreceptors and evidence by others that Schwann cells produce a variety of trophic factors (Reynolds and Woolf, 1993), we suggest that Schwann cells at mechanoreceptive terminal endings supply substances that are important for keeping sensory neurons alive during mechanoreceptor maturation. The apoptotic death and subsequent disappearance of the Schwann cells associated with these mechanoreceptors after neonatal denervation, and therefore a lack of supply of Schwann cell-derived substances, may partially explain why reinnervation of these structures is so poor.…”

Section: Discussionsupporting

confidence: 54%

Glial Growth Factor Rescues Schwann Cells of Mechanoreceptors from Denervation-Induced Apoptosis

1997

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Golgi tendon organs and Pacinian corpuscles are peripheral mechanoreceptors that disappear after denervation during a critical period in early postnatal development. Even if regeneration is allowed to occur, Golgi tendon organs do not reform, and the reformation of Pacinian corpuscles is greatly impaired. The sensory nerve terminals of both types of mechanoreceptors are closely associated with Schwann cells. Here we investigate the changes in the Schwann cells found in Golgi tendon organs and Pacinian corpuscles after nerve resection in the early neonatal period. We report that denervation induces the apoptotic death of these Schwann cells and that this apoptosis can be prevented by administration of a soluble form of neuregulin, glial growth factor 2. Schwann cells associated with these mechanoreceptors are immunoreactive for the neuregulin receptors erbB2, erbB3, and erbB4, and the sensory nerve terminals are immunoreactive for neuregulin. Our results suggest that Schwann cells in developing sensory end organs are trophically dependent on sensory axon terminals and that an axon-derived neuregulin mediates this trophic interaction. The denervation-induced death of mechanoreceptor Schwann cells is correlated with deficiencies in the re-establishment of these sensory end organs by regenerating axons.

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Section: Discussionsupporting

confidence: 54%

Glial Growth Factor Rescues Schwann Cells of Mechanoreceptors from Denervation-Induced Apoptosis

1997

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“…As development proceeds, axon bundles are progressively subdivided and segregated by premyelinating SC processes, and SC and axon establish a 1:1 ratio relationship prior to myelination (Reynolds and Woolf, 1993;Yao et al, 1990). In the rodent sciatic nerve during the first week of postnatal life, pre-myelinating SCs begin to myelinate their associated axons, together with a high level transcription of myelin-specific genes and a down-regulation of immature SC genes (Trapp et al, 1988;Zorick et al, 1996).…”

Section: Schwann Cell Developmentmentioning

confidence: 99%

Glial cells: Old cells with new twists

Ndubaku

Bellard

2008

Acta Histochemica

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SummaryBased on their characteristics and function -migration, neural protection, proliferation, axonal guidance and trophic effects -glial cells may be regarded as probably the most versatile cells in our body. For many years, these cells were considered as simply support cells for neurons. Recently, it has been shown that they are more versatile than previously believed -as true stem cells in the nervous system -and are important players in neural function and development. There are several glial cell types in the nervous system: the two most abundant are oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Although both of these cells are responsible for myelination, their developmental origins are quite different. Oligodendrocytes originate from small niche populations from different regions of the central nervous system, while Schwann cells develop from a stem cell population (the neural crest) that gives rise to many cell derivatives besides glia and which is a highly migratory group of cells.

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“…Lysosome-processed myelin debris then acts as an inducer and activator for resident macrophages [7,12,29]. Differentiated and activated Schwann cells and macrophages produce neurotrophic factors that accelerate axonal sprouting and outgrowth [21], while proliferating Schwann cells arrange themselves to form tubes to guide regenerating axons. Moreover, the area available for axonal outgrowth is increased as myelin debris clearance is accelerated [22].…”

Section: Discussionmentioning

confidence: 99%

Pre‐degenerated nerve shows enhanced regeneration after incremental elongation in rats

Hara

Tsujino

Abe

et al. 2004

Journal Orthopaedic Research

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Following nerve degeneration, we investigated effects of linear elongation on subsequent nerve regeneration in a total of 92 Wistar rats (weight 380430 g). The nerve was ligated at the midthigh and then elongated incrementally by a total of 15 mm by leg lengthening at a rate of 3 or 5 mm/day. Seven days after initiation of nerve elongation, the external fixator was removed and normal leg length was restored with internal fixation. Then a 10 mm nerve segment at the ligature site was excised, and the nerve was repaired with sutures (group D). At 2, 4, 6, and 8 weeks after nerve suturing, we examined transverse semi-thin nerve sections compared with group I (severed and repaired after leg lengthening without a nerve ligature) and control group (severed and repaired without leg lengthening). After lengthening at 3 mdday, nerve regeneration in group D was enhanced at 4 weeks. After lengthening at 5 mdday, nerve regeneration in group D also was enhanced at 6 and 8 weeks. Pre-degenerated nerve showed better regeneration after suturing than intact nerve. Elongation holds promise as an alternative to nerve grafting in treatment of nerve injury.

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Reciprocal Schwann cell-axon interactions

Cited by 144 publications

References 62 publications

Glial Growth Factor Rescues Schwann Cells of Mechanoreceptors from Denervation-Induced Apoptosis

Glial Growth Factor Rescues Schwann Cells of Mechanoreceptors from Denervation-Induced Apoptosis

Glial cells: Old cells with new twists

Pre‐degenerated nerve shows enhanced regeneration after incremental elongation in rats

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