Elsevier

Brain Research

Volume 182, Issue 1, 20 January 1980, Pages 180-185
Brain Research

Time course of the conditioning lesion effect on axonal regeneration

https://doi.org/10.1016/0006-8993(80)90842-2Get rights and content

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Cited by (98)

  • Transplantation of mesenchymal stem cells that overexpress NT-3 produce motor improvements without axonal regeneration following complete spinal cord transections in rats

    2018, Brain Research
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    Unfortunately, attempts to encourage long-distance axonal regeneration within the spinal cord have been met with many intracellular and extracellular complications. The inhibitory influences of myelin associated proteins, chondroitin sulfate proteoglycans, as well as an overall inability to initiate a growth response following axotomy, all contribute to the failure of regeneration within the central nervous system (Fernandes et al., 1999; Fitch and Silver, 1997; Forman et al., 1980; Lemons et al., 1999; Mason et al., 2003; Opatz et al., 2009; von Meyenburg et al., 1998; Woolf et al., 1990). Use of stem cells alone, or in combination with trophic factors, can stimulate axon regeneration when these are transplanted into animal models of SCI (Bregman et al., 1997, 1998, 2002; Coumans et al., 2001; Kumagai et al., 2013; Lu et al., 2004, 2005; Ruitenberg et al., 2005; Sasaki et al., 2009; Shang et al., 2011; Taylor et al., 2006; Tobias et al., 2003).

  • Crush injury to motor nerves in the G93A transgenic mouse model of amyotrophic lateral sclerosis promotes muscle reinnervation and survival of functionally intact nerve-muscle contacts

    2018, Neurobiology of Disease
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    A nerve crush injury caused a small but insignificant drop in numbers of MUs in a small sample of three extensor digitorum longus (EDL) muscles of SOD1G93A transgenic mice (Sharp et al., 2005) whilst a later study reported good survival of reinnervated neuromuscular junctions in the gastrocnemius muscle of SOD1G93A transgenic rats after a nerve crush injury (Franz et al., 2009). The increased survival was attributed to the crush injury as a conditioning lesion, a lesion that precedes or is coincident with a nerve injury (Bisby and Pollock, 1983; Dahlin and Kanje, 1992; Forman et al., 1980; Jacob and McQuarrie, 1993; McQuarrie, 1978, 1981; McQuarrie et al., 1977; McQuarrie and Jacob, 1991; Neumann et al., 2002). However, in the case of rodent models of ALS, many MUs were functionally intact at the time of the ‘conditioning’ crush lesion.

  • Defective axonal transport: A common pathological mechanism in inherited and acquired peripheral neuropathies

    2017, Neurobiology of Disease
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    In general, focus lies on improving nerve regeneration while reducing the degeneration of the distal part (Höke, 2006). Interestingly, regeneration of the nerve progresses at a rate similar to slow axonal transport, suggesting that axonal transport is a key determinant of the regeneration process (Forman et al., 1980). In contrast to the CNS, where retraction bulbs form at the tip of the cut axon, the microtubules of severed peripheral nerves maintain their initial organization (plus end towards the synapse/growth cone) and continue to serve as tracks for motor proteins that provide support for the growing axon (Ertürk et al., 2007).

  • Geldanamycin accelerated peripheral nerve regeneration in comparison to FK-506 in vivo

    2012, Neuroscience
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    Downstream programs of neurite outgrowth are initiated, including reorganization of microtubules and microfilaments, upregulated expression of GAP-43 (a growth cone path-finding protein associated with nerve growth and plasticity) (Gold et al., 1998; Madsen et al., 1998), and potential crosstalk with signal transduction pathways for neurotrophic factors like NGF (Gold et al., 1999). As has been noted previously (Yan et al., 2011), the first injury in the saphenous nerve crush model induces a pre-conditioned nerve injury state that enhances the regenerative response to the second crush injury (McQuarrie, 1978; Forman et al., 1980; Sjoberg and Kanje, 1990; Lankford et al., 1998). Like FK-506, GA provides an additional benefit to nerve regeneration above that of pre-conditioning.

  • The fundamental role of subcellular topography in peripheral nerve repair therapies

    2012, Biomaterials
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    This type of conditioning lesion has been used as a model to study intrinsic regenerative potential. Further conditioning lesion studies showed that inflammatory cells in the injured areas may enhance axonal regeneration [34], and that there may be a time limit in the conditioning lesion's ability to enhance axonal regeneration of central nervous system axons [35]. These results suggest that although conditioning lesions can increase intrinsic regenerative capacity of central axons, this effect has a time dependence.

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We wish to thank Dr. R. C. Bailey, Dr. Louis D. Homer and James Summe for help in the statistical analysis of the data, and Mrs. Helen Wise for typing the manuscript

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Present address: Department of Anatomy, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, U.S.A.

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