Failure of reinnervation of Pacinian corpuscle after nerve crush

1973 ◽  
Vol 23 (4) ◽  
pp. 338-341 ◽  
Author(s):  
A. Krishnamurti ◽  
R. Kanagasuntheram ◽  
S. Vij
Keyword(s):  
Pacinian Corpuscle ◽  
Nerve Crush

Muscle-derived GDNF facilitates motor nerve recovery following sciatic nerve crush injury

2007 ◽  
Vol 205 (3) ◽  
pp. S92
Author(s):  
Terence M. Myckatyn ◽  
Christina Kenney ◽  
Alice Tong ◽  
Jessica Duan ◽  
Daniel Hunter ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Motor Nerve ◽  
Crush Injury ◽  
Sciatic Nerve Crush ◽  
Nerve Crush ◽  
Nerve Recovery ◽  
Nerve Crush Injury

scholarly journals Changes in intra-axonal calcium distribution following nerve crush

1986 ◽  
Vol 17 (5) ◽  
pp. 449-467 ◽  
Author(s):  
Marina Mata ◽  
Julie Staple ◽  
David J. Fink
Keyword(s):  
Nerve Crush ◽  
Calcium Distribution

scholarly journals Blocking LINGO-1 in vivo reduces degeneration and enhances regeneration of the optic nerve

2016 ◽  
Vol 2 ◽  
pp. 205521731664170 ◽  
Author(s):  
Melissa M Gresle ◽  
Yaou Liu ◽  
Trevor J Kilpatrick ◽  
Dennis Kemper ◽  
Qi-Zhu Wu ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Axonal Regeneration ◽  
Antibody Therapy ◽  
Experimental Models ◽  
Therapeutic Effects ◽  
Axonal Loss ◽  
Nerve Crush ◽  
Acute Optic Neuritis ◽  
Injury Models

Background Two ongoing phase II clinical trials (RENEW and SYNERGY) have been developed to test the efficacy of anti-LINGO-1 antibodies in acute optic neuritis and relapsing forms of multiple sclerosis, respectively. Across a range of experimental models, LINGO-1 has been found to inhibit neuron and oligodendrocyte survival, axon regeneration, and (re)myelination. The therapeutic effects of anti-LINGO-1 antibodies on optic nerve axonal loss and regeneration have not yet been investigated. Objective In this series of studies we investigate if LINGO-1 antibodies can prevent acute inflammatory axonal loss, and promote axonal regeneration after injury in rodent optic nerves. Methods The effects of anti-LINGO-1 antibody on optic nerve axonal damage were assessed using rodent myelin oligodendrocyte glycoprotein experimental autoimmune encephalomyelitis (EAE), and its effects on axonal regeneration were assessed in optic nerve crush injury models. Results In the optic nerve, anti-LINGO-1 antibody therapy was associated with improved optic nerve parallel diffusivity measures on MRI in mice with EAE and reduced axonal loss in rat EAE. Both anti-LINGO-1 antibody therapy and the genetic deletion of LINGO-1 reduced nerve crush-induced axonal degeneration and enhanced axonal regeneration. Conclusion These data demonstrate that LINGO-1 blockade is associated with axonal protection and regeneration in the injured optic nerve.

Functional Recovery and Vitamin E Level Following Sciatic Nerve Crush Injury in Normal and Diabetic Rats

1998 ◽  
Vol 96 (3-4) ◽  
pp. 245-254 ◽  
Author(s):  
Khalaf Al Moutaery ◽  
Mohammed Arshaduddin ◽  
Mohammad Tariq ◽  
Saleh Al Deeb
Keyword(s):  
Vitamin E ◽  
Sciatic Nerve ◽  
Functional Recovery ◽  
Diabetic Rats ◽  
Crush Injury ◽  
Sciatic Nerve Crush ◽  
Nerve Crush ◽  
Nerve Crush Injury

scholarly journals The Parameters of Transcutaneous Electrical Nerve Stimulation Are Critical to Its Regenerative Effects When Applied Just after a Sciatic Crush Lesion in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Diana Cavalcante Miranda de Assis ◽  
Êmyle Martins Lima ◽  
Bruno Teixeira Goes ◽  
João Zugaib Cavalcanti ◽  
Alaí Barbosa Paixão ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Nerve Stimulation ◽  
Transcutaneous Electrical Nerve Stimulation ◽  
Peripheral Nerve Regeneration ◽  
Light And Electron Microscopy ◽  
Nerve Crush ◽  
Electrical Nerve Stimulation ◽  
The Right ◽  
Crush Lesion

We investigated the effect of two frequencies of transcutaneous electrical nerve stimulation (TENS) applied immediately after lesion on peripheral nerve regeneration after a mouse sciatic crush injury. The animals were anesthetized and subjected to crushing of the right sciatic nerve and then separated into three groups: nontreated, Low-TENS (4 Hz), and High-TENS (100 Hz). The animals of Low- and High-TENS groups were stimulated for 2 h immediately after the surgical procedure, while the nontreated group was only positioned for the same period. After five weeks the animals were euthanized, and the nerves dissected bilaterally for histological and histomorphometric analysis. Histological assessment by light and electron microscopy showed that High-TENS and nontreated nerves had a similar profile, with extensive signs of degeneration. Conversely, Low-TENS led to increased regeneration, displaying histological aspects similar to control nerves. High-TENS also led to decreased density of fibers in the range of 6–12 μm diameter and decreased fiber diameter and myelin area in the range of 0–2 μm diameter. These findings suggest that High-TENS applied just after a peripheral nerve crush may be deleterious for regeneration, whereas Low-TENS may increase nerve regeneration capacity.

scholarly journals Laminin γ1 is critical for Schwann cell differentiation, axon myelination, and regeneration in the peripheral nerve

2003 ◽  
Vol 163 (4) ◽  
pp. 889-899 ◽  
Author(s):  
Zu-Lin Chen ◽  
Sidney Strickland
Keyword(s):  
Schwann Cells ◽  
Peripheral Nerves ◽  
Matrix Proteins ◽  
Myelin Proteins ◽  
Sciatic Nerve Crush ◽  
Similar Reduction ◽  
Nerve Crush ◽  
And Function ◽  
Schwann Cell Differentiation

Laminins are heterotrimeric extracellular matrix proteins that regulate cell viability and function. Laminin-2, composed of α2, β1, and γ1 chains, is a major matrix component of the peripheral nervous system (PNS). To investigate the role of laminin in the PNS, we used the Cre–loxP system to disrupt the laminin γ1 gene in Schwann cells. These mice have dramatically reduced expression of laminin γ1 in Schwann cells, which results in a similar reduction in laminin α2 and β1 chains. These mice exhibit motor defects which lead to hind leg paralysis and tremor. During development, Schwann cells that lack laminin γ1 were present in peripheral nerves, and proliferated and underwent apoptosis similar to control mice. However, they were unable to differentiate and synthesize myelin proteins, and therefore unable to sort and myelinate axons. In mutant mice, after sciatic nerve crush, the axons showed impaired regeneration. These experiments demonstrate that laminin is an essential component for axon myelination and regeneration in the PNS.

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