Schwann cells reposition a peripheral nerve to isolate it from postembryonic remodeling of its targets

Raphael, Alya R.; Perlin, Julie R.; Talbot, William S.

doi:10.1242/dev.057521

Cited by 26 publications

(29 citation statements)

References 41 publications

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“…To determine whether nrg1 z26 mutant nerves resemble erbb mutant nerves at the ultrastructural level, we examined transverse sections of the PLLn by transmission electron microscopy (TEM). As in other mutants lacking Schwann cells (Raphael et al, 2010;Voas et al, 2009) …”

Section: Ultrastructural Analysis Of Nrg1 Type III Mutantssupporting

confidence: 54%

“…The PLLn initially grows out within the epidermis above the basement membrane, and Schwann cells are required for the nerve to transition to its mature location beneath this basement membrane (Raphael et al, 2010). At 5 dpf the nerve is normally located beneath the basement membrane and Schwann cells have begun to myelinate axons ( Fig.…”

Section: Ultrastructural Analysis Of Nrg1 Type III Mutantsmentioning

confidence: 99%

“…3A,AЈ; n10). In the absence of Schwann cells, erbb mutant nerves remain in the epidermis and become 4641 RESEARCH ARTICLE Nrg1 and Schwann cell migration defasciculated (Raphael et al, 2010). To determine whether nrg1 z26 mutant nerves resemble erbb mutant nerves at the ultrastructural level, we examined transverse sections of the PLLn by transmission electron microscopy (TEM).…”

Section: Ultrastructural Analysis Of Nrg1 Type III Mutantsmentioning

confidence: 99%

“…In zebrafish, some neural crest cells coalesce at the ganglion of the posterior lateral line nerve (PLLn) and become Schwann cell precursors that migrate with growing axons (Gilmour et al, 2002;Grant et al, 2005). In the PLLn, migrating Schwann cells each associate with many axons and bundle them into one fascicle (Gilmour et al, 2002;Raphael et al, 2010). After axonal and Schwann cell migration is completed, Schwann cells proliferate to generate the large number of cells required to myelinate the many axonal segments in a nerve.…”

Section: Introductionmentioning

confidence: 99%

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Neuronal Neuregulin 1 type III directs Schwann cell migration

et al. 2011

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SUMMARYDuring peripheral nerve development, each segment of a myelinated axon is matched with a single Schwann cell. Tight regulation of Schwann cell movement, proliferation and differentiation is essential to ensure that these glial cells properly associate with axons. ErbB receptors are required for Schwann cell migration, but the operative ligand and its mechanism of action have remained unknown. We demonstrate that zebrafish Neuregulin 1 (Nrg1) type III, which signals through ErbB receptors, controls Schwann cell migration in addition to its previously known roles in proliferation and myelination. Chimera analyses indicate that ErbB receptors are required in all migrating Schwann cells, and that Nrg1 type III is required in neurons for migration. Surprisingly, expression of the ligand in a few axons is sufficient to induce migration along a chimeric nerve constituted largely of nrg1 type III mutant axons. These studies also reveal a mechanism that allows Schwann cells to fasciculate axons regardless of nrg1 type III expression. Time-lapse imaging of transgenic embryos demonstrated that misexpression of human NRG1 type III results in ectopic Schwann cell migration, allowing them to aberrantly enter the central nervous system. These results demonstrate that Nrg1 type III is an essential signal that controls Schwann cell migration to ensure that these glia are present in the correct numbers and positions in developing nerves.

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Section: Ultrastructural Analysis Of Nrg1 Type III Mutantssupporting

confidence: 54%

Section: Ultrastructural Analysis Of Nrg1 Type III Mutantsmentioning

confidence: 99%

Section: Ultrastructural Analysis Of Nrg1 Type III Mutantsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neuronal Neuregulin 1 type III directs Schwann cell migration

et al. 2011

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“…1G,H). The PLLn undergoes dramatic 3169 RESEARCH ARTICLE Role of Gpr126 in myelination postembryonic remodeling (Ghysen and Dambly-Chaudière, 2007;Raphael et al, 2010), with many axons branching off to innervate sensory neuromasts. Therefore, it is likely that the difference between seven and four myelinated axons at 9 dpf and 30 dpf, respectively, reflects the changing anatomy of the nerve during that period rather than a loss of myelinated axons.…”

Section: Gpr126 Signaling Activity Is Required Specifically At the Onmentioning

confidence: 99%

Analysis of Gpr126 function defines distinct mechanisms controlling the initiation and maturation of myelin

Glenn

Talbot

2013

Development

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SUMMARYIn peripheral nerves, Schwann cells form the myelin sheath, which allows the efficient propagation of action potentials along axons. The transcription factor Krox20 regulates the initiation of myelination in Schwann cells and is also required to maintain mature myelin. The adhesion G protein-coupled receptor (GPCR) Gpr126 is essential for Schwann cells to initiate myelination, but previous studies have not addressed the role of Gpr126 signaling in myelin maturation and maintenance. Through analysis of Gpr126 in zebrafish, we define two distinct mechanisms controlling the initiation and maturation of myelin. We show that gpr126 mutant Schwann cells elaborate mature myelin sheaths and maintain krox20 expression for months, provided that the early signaling defect is bypassed by transient elevation of cAMP. At the onset of myelination, Gpr126 and protein kinase A (PKA) function as a switch that allows Schwann cells to initiate krox20 expression and myelination. After myelination is initiated, krox20 expression is maintained and myelin maturation proceeds independently of Gpr126 signaling. Transgenic analysis indicates that the Krox20 cis-regulatory myelinating Schwann cell element (MSE) becomes active at the onset of myelination and that this activity is dependent on Gpr126 signaling. Activity of the MSE declines after initiation, suggesting that other elements are responsible for maintaining krox20 expression in mature nerves. We also show that elevated cAMP does not initiate myelination in the absence of functional Neuregulin 1 (Nrg1) signaling. These results indicate that the mechanisms regulating the initiation of myelination are distinct from those mediating the maturation and maintenance of myelin.

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Curcumin Ameliorates the Experimental Diabetic Peripheral Neuropathy through Promotion of NGF Expression in Rats

Zhang

Lin

Sun

et al. 2022

Chemistry & Biodiversity

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Increasing evidence suggested that inhibiting the apoptosis of Schwann cells (SCs) and promoting nerve growth factor (NGF) expression in sciatic nerves play key roles in preventing the onset of diabetic peripheral neuropathy (DPN). Curcumin, a primary bioactive substance in turmeric with multiple characteristics, has been shown to have many therapeutic effects in a variety of diseases. However, curcumin is poorly studied in the DPN models. We aimed to explore the therapeutic benefits and underlying mechanism of curcumin in high fat/sugar diets joint streptozotocin (STZ)‐induced DPN rat models. Sprague‐Dawley (SD) rats were divided into five groups (6 rats per group), control group, DPN group, Curcumin groups (50, 100, and 150 mg/kg). Curcumin was administered intragastrically once per day for 4 continuous weeks. Body weight (BW) and fasting blood glucose (FBG) were monitored in all groups. The mechanical withdraw threshold (MWT) was measured. We also assessed neuropathic change by testing nerve conductance velocity (NCV) in sciatic nerves. TEM was applied to observe the sciatic nerves ultrastructure. The SCs apoptosis in sciatic nerves was stained using TUNEL kit. NGF contents in sciatic nerves and serum were detected using western blotting and ELISA analysis. The results showed curcumin had no obvious effect on the BW and FBG change. Curcumin (100 and 150 mg/kg) attenuated the MWT, NCV, and sciatic nerves ultrastructure in DPN rats. Curcumin (50, 100 and 150 mg/kg) reduced SCs apoptosis in sciatic nerves. In addition, curcumin at 150 mg/kg had the best efficacy in increasing protein expression of NGF in sciatic nerves and serum NGF level. Our work demonstrated that curcumin has neuroprotective effects for the treatment of DPN.

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Schwann cells reposition a peripheral nerve to isolate it from postembryonic remodeling of its targets

Cited by 26 publications

References 41 publications

Neuronal Neuregulin 1 type III directs Schwann cell migration

Neuronal Neuregulin 1 type III directs Schwann cell migration

Analysis of Gpr126 function defines distinct mechanisms controlling the initiation and maturation of myelin

Curcumin Ameliorates the Experimental Diabetic Peripheral Neuropathy through Promotion of NGF Expression in Rats

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