A comparative study of the effects of chronic axotomy, crush lesion and re-anastomosis of the rat sural nerve on horseradish peroxidase labelling of primary sensory neurons

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

“…The number of neurones labelled by this tracer could be misleading, however, if regenerating neurones change their 14 capacity to uptake and transport tracers as compared to normal (Peyronnard et al, 1986(Peyronnard et al, , 1988), or if labelling by the first tracer interferes with the uptake of the second tracer (Puigdellívol et al, 2000). No significant differences in the numbers of labelled DRG neurones were found for the three tracers used in this study after single application to the previously transected nerve after the regeneration period, indicating that there was no major difference in the uptake, transport or accumulation capacity between tracers.…”

“…Finally, the absence of functional alterations of labelled cells in vivo has been considered to be strong evidence for lack of toxicity, as was shown by the maintenance of homeostatic parameters after labelling of magnocellular neuroendocrine cells with Evans Blue (Weiss and Cobbett, 1992). In addition to toxic effects, the altered metabolism of the neuron after injury may change the uptake and transport mechanisms, as has been shown for horseradishperoxidase (Peyronnard et al, 1986(Peyronnard et al, , 1988.…”

Regeneration of Unmyelinated Axons After Injury of Mammalian Peripheral Nerve

“…This is so after crush (Peyronnard et al 1988;Toft et al 1988); after cutting a nerve and allowing it to regenerate -with or without microsurgical repair - (Horch & Lisney, 1981;Carter & Lisney, 1987;Lisney, 1988;Peyronnard et al 1988;Pover & Lisney, 1988); after removing a sizeable piece of nerve and carrying out a repair (Gibby, Koeber & Horch, 1983;Pover & Lisney, 1988; and after sectioning a nerve and taking deliberate steps to make a stump neuroma form (Janig & McLachlan, 1984;Peyronnard et al 1986Peyronnard et al a, 1988. It is even the case when the proximal stump of a cut nerve is united with the distal stump of another nerve of different size (Peyronnard et al 1988). Either neurones with myelinated axons do not die after injury or those that survive sprout to produce a total complement of myelinated axons in the proximal stump that, on average, matches the original number.…”

“…sural, saphenous, superficial peroneal) 70-80 % of the unmyelinated axons are afferent and the remaining 20-30 % postganglionic sympthetics (Blumberg & Janig, 1982;Chad, Bradley, Rasool, Good, Reichlin & Zivin, 1983;Langford, 1983;McLachlan & Janig, 1983;Schmalbruch, 1986; Sittiracha & McLachlan, 1986;Lisney, 1987;Baron, Janig & Kollmann, 1988;Peyronnard et al 1988). …”

“…They maintain that a proportion of chronically axotomized neurones survive injury but because of some dysfunction they are unable to take up HRP and/or transport it back to their cell body. Where damaged nerves are free to regenerate and have an opportunity to re-establish a connection with a peripheral target this dysfunction does not arise (Peyronnard et al 1988). …”