Effect of conditioning lesions on regeneration of goldfish optic axons: time course of the cell body reaction to axotomy

Reich, Jeffrey; Burmeister, Donald W.; Schmidt, John T.; Grafstein, Bernice

doi:10.1016/0006-8993(90)90604-a

Cited by 9 publications

(6 citation statements)

References 18 publications

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“…Even the axons that are routed into the remaining tectal lobe do not begin to invade the tectal tissue until about 4 weeks, which is 2 weeks later than normal, and do not cover the tectum completely until 6-8 weeks, compared to about 4 weeks in the normal. Thus, in many of the axons, the period of elongation lasts longer than usual, and the onset of synaptogenesis is thereby delayed (Reich et al, 1990). Many ofthe regenerated projections are abnormally located (Lo and Levine, 1980); however, most ganglion cells apparently have branches that cross into the remaining tectal lobe between 4 and 10 weeks after tectal lobe ablation (D. W. Burmeister and B. Grafstein, unpublished observations).…”

Section: Class D Weeks Weeksmentioning

confidence: 99%

Effect of target removal on goldfish optic nerve regeneration: analysis of fast axonally transported proteins

1990

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How is axonal transport in regenerating neurons affected by contact with their synaptic target? We investigated whether removing the target (homotopic) lobe of the goldfish optic tectum altered the incorporation of 3H-proline into fast axonally transported proteins in the regenerating optic nerve. Regeneration was induced either by an optic tract lesion (to reveal the changes in the original axon segment that remained connected to the cell body) or by an optic nerve lesion (to reveal the changes in the newly formed axon segment). Of 26 proteins analyzed by 2-dimensional gel electrophoresis and fluorography, all but one showed increased labeling as a result of tectal lobe ablation. By 2 d after the lesion, significantly increased labeling of some proteins was seen with a 6-hr labeling interval, but not with a 24-hr labeling interval. This is probably indicative of an increased velocity of transport, which may have been a nonspecific consequence of the surgery. Otherwise, tectal lobe removal had relatively little effect until 3 weeks, when there was a transitory increase in labeling of transported proteins in the new axon segments of the tectum-ablated animals. Beginning at 5 weeks, tectal lobe ablation caused considerably higher labeling of many of the proteins in the original axon segments. Because this was seen with both 6-hr and 24-hr labeling intervals, it is probably indicative of increased protein synthesis. The increased synthesis lasted until at least 12 weeks, though some proteins were beginning to show a diminished effect at this time. In the late stages of regeneration (8-12 weeks), there was also increased labeling of proteins in the new axon segments as a result of the absence of the target tectal lobe. This included a disproportionately large increase in the relative contribution of cytoskeletal proteins and of protein 4, which is the goldfish equivalent of the growth-associated protein GAP- 43 (neuromodulin). We conclude that, after the regenerating axons begin to innervate the tectum, the expression of most of the proteins in fast axonal transport is down-regulated by interaction between the axons and their target. However, the changes in expression may be preceded by a modulation of the turnover and/or deposition of proteins in the newly formed axon segment.

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Section: Class D Weeks Weeksmentioning

confidence: 99%

Effect of target removal on goldfish optic nerve regeneration: analysis of fast axonally transported proteins

1990

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“…Local environment-Other studies suggest that, after a CL, degenerative tissue in the vicinity of the lesion makes it physically easier for growth cones to elongate in this region, and the release of growth factors by glia and other cells might enhance outgrowth of axons (Bisby and Pollock, 1983; Bisby and Keen, 1985; Cho and So, 1989;Edbladh and Edstrom, 1989;Reich et al, 1990;Sjöberg and Kanje, 1990;Lu and Richardson, 1991). For example, when glia and other nonneuronal cells are temporarily frozen around an injury site in the rat sciatic nerve, CLs do not enhance axonal regeneration (Sjöberg and Kanje, 1990).…”

Section: Mechanisms For Cls From Studies In Other Animalsmentioning

confidence: 99%

“…Some experiments suggest that the cell body response plays a major role in the CL effect (McQuarrie and Grafstein, 1982;McQuarrie, 1985; McQuarrie, 1991, 1993;Tetzlaff et al, 1996). For example, when frogs are maintained at 15°C, which is thought to inhibit the cell body response, CLs of the sciatic nerve do not produce enhanced axonal regeneration compared to the significant CL effect that occurs at 25°C (Carlsen, 1983).Local environment-Other studies suggest that, after a CL, degenerative tissue in the vicinity of the lesion makes it physically easier for growth cones to elongate in this region, and the release of growth factors by glia and other cells might enhance outgrowth of axons (Bisby and Pollock, 1983; Bisby and Keen, 1985; Cho and So, 1989;Edbladh and Edstrom, 1989;Reich et al, 1990;Sjöberg and Kanje, 1990;Lu and Richardson, 1991). For example, when glia and other nonneuronal cells are temporarily frozen around an injury site in the rat sciatic nerve, CLs do not enhance axonal regeneration (Sjöberg and Kanje, 1990).…”

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confidence: 99%

“…CL effects have also been found to enhance axonal regeneration of motoneurons in the facial nerves of rats (Tetzlaff et al, 1996). In goldfish with a CL of the optic nerve, after a subsequent more proximal nerve lesion, the initial delay of axonal regeneration of retinal ganglion cells is reduced, and the rate of axonal outgrowth is increased (Lanners and Grafstein, 1980;Grafstein, 1981, 1982;Reich et al, 1990). Finally, in "old" rats, CLs induce axons of motoneurons to regenerate at growth rates typical of those in "young" animals (Jacob and Croes, 1998).…”

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confidence: 99%

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Conditioning lesions enhance axonal regeneration of descending brain neurons in spinal‐cord‐transected larval lamprey

Zhang¹,

Palmer²,

McClellan³

2004

J of Comparative Neurology

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In larval lamprey, with increasing recovery times after a transection of the rostral spinal cord, there is a gradual recovery of locomotor behavior, and descending brain neurons regenerate their axons for progressively greater distances below the transection site. In the present study, spinal cord "conditioning lesions" (i.e., transections) were performed in the spinal cord at 30% body length (BL; normalized distance from the head) or 50% BL. After various "lesion delay times" (D), a more proximal spinal cord "test lesion" (i.e., transection) was performed at 10% BL, and then, after various recovery times (R), horseradish peroxidase was applied to the spinal cord at 20% BL to determine the extent of axonal regeneration of descending brain neurons. Conditioning lesions at 30% BL, lesion delay times of 2 weeks, and recovery times of 4 weeks (D-R = 2-4 group) resulted in a significant enhancement of axonal regeneration for the total numbers of descending brain neurons as well as neurons in certain brain cell groups compared to control animals without conditioning lesions. Experiments with hemiconditioning lesions, which reduce interanimal variability, confirmed that conditioning lesions do significantly enhance axonal regeneration and indicate that axotomy rather than diffusible factors released at the injury site is primarily involved in this enhancement. Results from the present study suggest that conditioning lesions "prime" descending brain neurons via cell body responses and enhance subsequent axonal regeneration, probably by reducing the initial delay and/or increasing the initial rate of axonal outgrowth. Indexing termsaxotomy; reticulospinal neurons; spinal cord injury; conditioning lesion; test lesion When neurons are axotomized, they often are "primed" for possible subsequent axonal regeneration. If the axons of these neurons then receive a second "test lesion," often proximal to the first "conditioning lesion" (CL), regeneration can be enhanced compared with that of neurons without previous CLs. This phenomenon of enhanced axonal regeneration is called the "CL effect" (Forman et al., 1980). Because most studies of CL effects have been performed on nerves (e.g., sciatic nerve or optic nerve), crush injuries usually are employed for both the conditioning and the test lesions.After an initial CL, there are a series of morphological, physiological, and biochemical changes in axotomized neurons (McQuarrie and Grafstein, 1982;Redshaw and Bisby, 1987 Perry et al., 1987;Jacob and McQuarrie, 1991;Tetzlaff et al., 1996). Investigating the effects of CLs potentially might clarify the mechanisms that regulate neural regeneration, and it might then be possible to manipulate these mechanisms to enhance axonal regeneration. For example, a CL of the peripheral branch of neurons in dorsal root ganglia (DRG) raises cAMP levels and promotes axonal regeneration of the central branches of these neurons, and this effect can be mimicked by injection of cAMP in DRG (Qiu et al., 2002).The effects of CLs have been invest...

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“…S.W. You et al Axonal regeneration can be accelerated by an initial or conditioning lesion in the PNS axons of rodents (McQuarrie et al, 1977;McQuarrie, 1978;Wells & Bernstein, 1978) and the optic axons of lower vertebrates (Brock, 1978;Lanners & Grafstein, 1980;Mc-Quarrie & Grafstein, 1981;Reich et al, 1990). These axons have been shown to regenerate vigorously following a single axotomy.…”

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confidence: 99%

Axonal regeneration of retinal ganglion cells after optic nerve pre-lesions and attachment of normal or pre-degenerated peripheral nerve grafts

et al. 2002

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Axonal regeneration of retinal ganglion cells (RGCs) into a normal or pre-degenerated peripheral nerve graft after an optic nerve pre-lesion was investigated. A pre-lesion performed 1-2 weeks before a second lesion has been shown to enhance axonal regeneration in peripheral nerves (PN) but not in optic nerves (ON) in mammals. The lack of such a beneficial pre-lesion effect may be due to the long delay (1-6 weeks) between the two lesions since RGCs and their axons degenerate rapidly 1-2 weeks following axotomy in adult rodents. The present study examined the effects of the proximal and distal ON pre-lesions with a shortened delay (0-8 days) on axonal regeneration of RGCs through a normal or pre-degenerated PN graft. The ON of adult hamsters was transected intraorbitally at 2 mm (proximal lesion) or intracranially at 7 mm (distal lesion) from the optic disc. The pre-lesioned ON was re-transected at 0.5 mm from the disc after 0, 1, 2, 4, or 8 days and a normal or a pre-degenerated PN graft was attached onto the ocular stump. The number of RGCs regenerating their injured axons into the PN graft was estimated by retrograde labeling with FluoroGold 4 weeks after grafting. The number of regenerating RGCs decreased significantly when the delay-time increased in animals with both the ON pre-lesions (proximal or distal) compared to control animals without an ON pre-lesion. The proximal ON pre-lesion significantly reduced the number of regenerating RGCs after a delay of 8 days in comparison with the distal lesion. However, this adverse effect can be overcome, to some degree, by a pre-degenerated PN graft applied 2, 4, or 8 days after the distal ON pre-lesion enhanced more RGCs to regenerate than the normal PN graft. Thus, in order to obtain the highest number of regenerating RGCs, a pre-degenerated PN should be grafted immediately after an ON lesion.

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Effect of conditioning lesions on regeneration of goldfish optic axons: time course of the cell body reaction to axotomy

Cited by 9 publications

References 18 publications

Effect of target removal on goldfish optic nerve regeneration: analysis of fast axonally transported proteins

Effect of target removal on goldfish optic nerve regeneration: analysis of fast axonally transported proteins

Conditioning lesions enhance axonal regeneration of descending brain neurons in spinal‐cord‐transected larval lamprey

Axonal regeneration of retinal ganglion cells after optic nerve pre-lesions and attachment of normal or pre-degenerated peripheral nerve grafts

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