Neuronal loss in lumbar dorsal root ganglia after proximal compared to distal sciatic nerve resection: a quantitative study in the rat

Ygge, Jan

doi:10.1016/0006-8993(89)91497-2

Cited by 105 publications

(54 citation statements)

References 11 publications

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“…This reduction might also to some degree be attributed to an inability of the second tracer to label a certain population of surviving neurones, or to fading of the first tracer in nonregenerating but surviving neurones. Nevertheless, the percentages of cell loss estimated by this method are similar to the range of neuronal death in DRG after peripheral nerve injury reported in other studies (Arvidsson et al, 1986;Himes and Tessler, 1989;Ygge, 1989;Vestergaard et al, 1997;Ljungberg et al, 1999).…”

Section: Labelling With the First Tracer: Neuronal Death Versus Tracesupporting

confidence: 87%

“…By analogy to findings in the DRGs (Ygge and Aldskogius, 1984;Arvidsson et al, 1986;Groves et al, 1997), an increased amount of neuronal disappearence in the motor columns could take place if very long survival times were studied. Furthermore, the degree of motoneuronal (Martin et al, 1999) and DRG neuronal (Ygge, 1989) death after axonal injury in adult mammals was found to be mainly dependent on the severity of the injury and on the distance from the axonal injury to the neuronal body.…”

Section: Labelling With the First Tracer: Neuronal Death Versus Tracementioning

confidence: 96%

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On the use of fast blue, fluoro-gold and diamidino yellow for retrograde tracing after peripheral nerve injury: uptake, fading, dye interactions, and toxicity

Puigdellı́vol-Sánchez

Valero‐Cabré

Prats-Galino

et al. 2002

Journal of Neuroscience Methods

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The usefulness of three retrograde fluorescent dyes for tracing injured peripheral axons was investigated. The rat sciatic was transected bilaterally and the proximal end briefly exposed to either Fast Blue (FB), Fluoro-Gold (FG) or to Diamidino Yellow (DY) on the right side, and to saline on the left side, respectively. The nerves were then resutured and allowed to regenerate.Electrophysiological tests three months later showed similar latencies and amplitudes of evoked muscle and nerve action potentials between tracer groups. The nerves were then cut distal to the original injury and exposed to a second (different) dye. Five days later, retrogradely labelled neurones were counted in the dorsal root ganglia (DRGs) and spinal cord ventral horn. The number of neurones labelled by the first tracer was similar for all three dyes in the DRG and ventral horn except for FG, which labelled fewer motoneurones. When used as second tracer, DY labelled fewer neurones than FG and FB in some experimental situations. The total number of neurones labelled by the first and/or second tracer was reduced by about 30% compared to controls. The contributions of cell death as well as different optional tracer combinations for studies of nerve regeneration are discussed.

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Section: Labelling With the First Tracer: Neuronal Death Versus Tracesupporting

confidence: 87%

Section: Labelling With the First Tracer: Neuronal Death Versus Tracementioning

confidence: 96%

On the use of fast blue, fluoro-gold and diamidino yellow for retrograde tracing after peripheral nerve injury: uptake, fading, dye interactions, and toxicity

Puigdellı́vol-Sánchez

Valero‐Cabré

Prats-Galino

et al. 2002

Journal of Neuroscience Methods

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“…They mediate many of the typical biochemical and morphological changes characteristic of cells undergoing apoptosis. The extent of apoptosis of DRG cells after axotomy varies with the species and with the level of the injury, but may reach 50% in rodent models (Dahlin, 2006;Ygge, 1989). Apoptosis is more severe and rapid in sensory than motor neurons after peripheral injuries.…”

Section: Nerve Regenerationmentioning

confidence: 99%

Evaluation and management of peripheral nerve injury

Campbell

2008

Clinical Neurophysiology

592

462

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Common etiologies of acute traumatic peripheral nerve injury (TPNI) include penetrating injury, crush, stretch, and ischemia. Management of TPNI requires familiarity with the relevant anatomy, pathology, pathophysiology, and the surgical principles, approaches and concerns. Surgical repair of TPNI is done at varying time intervals after the injury, and there are a number of considerations in deciding whether and when to operate. In neurapraxia, the compound muscle and nerve action potentials on stimulating distal to the lesion are maintained indefinitely; stimulation above the lesion reveals partial or complete conduction block. The picture in axonotmesis and neurotmesis depends on the time since injury. The optimal timing for an electrodiagnostic study depends upon the clinical question being asked. Although conventional teaching usually holds that an electrodiagnostic study should not be done until about 3 weeks after the injury, in fact a great deal of important information can be obtained by studies done in the first week. Proximal nerve injuries are problematic because the long distance makes it difficult to reinnervate distal muscles before irreversible changes occur. Decision making regarding exploration must occur more quickly, and exploration using intraoperative nerve action potential recording to guide the choice of surgical procedure is often useful.

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“…There is a larger loss of sensitive neurons at proximal resections compared to the distal resections in the nerve. At proximal lesions the response of pericarium is more intense and can exceed its synthesis capacity resulting in neuronal death (Ygge 1989).…”

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confidence: 99%

Pharmacological immunomodulation enhances peripheral nerve regeneration

et al. 2007

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To assess the effect of N-Acetylmuramyl-L-Alanyl-D-Isoglutamine MDP topically administrated on the regenerating peripheral neurons, twelve male C57BL/6J adult mice were equally distributed into three groups. Four mice underwent unilateral sciatic nerve transection and polyethylene tubulization, with a 4mm gap between the proximal and distal nerve stumps and were implanted with collagen + PBS (COL). Other four animals underwent the same surgical procedure but received collagen + MDP (COL/MDP) inside the prosthesis. Four animals were not operated and served as control group (NOR). After 4 weeks, the regenerated nerve cables were processed for total myelinated axon counting and myelinated fiber diameter measurement. The L5 dorsal root ganglion (DRG) was also removed and sectioned for sensory neurons counting and measurement. The results revealed significant difference (p<0.05) in axonal counting among the groups NOR (4,355±32), COL (1,869±289) and COL/MDP (2,430±223). There was a significant reduction in the axonal diameter in the operated groups (COL=3.38µm±1.16 and COL/MDP=3.54µm±1.16) compared to NOR (6.19µm±2.45). No difference was found in the number of DRG neurons between the experimental groups (COL=564±51; COL/MDP=514±56), which presented fewer sensory neurons compared to NOR (1,097±142). Data obtained indicate that locally applied MDP stimulates peripheral nerve regeneration in mice.

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Neuronal loss in lumbar dorsal root ganglia after proximal compared to distal sciatic nerve resection: a quantitative study in the rat

Cited by 105 publications

References 11 publications

On the use of fast blue, fluoro-gold and diamidino yellow for retrograde tracing after peripheral nerve injury: uptake, fading, dye interactions, and toxicity

On the use of fast blue, fluoro-gold and diamidino yellow for retrograde tracing after peripheral nerve injury: uptake, fading, dye interactions, and toxicity

Evaluation and management of peripheral nerve injury

Pharmacological immunomodulation enhances peripheral nerve regeneration

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