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Electrophysiological study of conditioning lesion effects of rat sciatic nerve regeneration following either prior section or freeze ii. blocking by prior tenotomy


, : Electrophysiological study of conditioning lesion effects of rat sciatic nerve regeneration following either prior section or freeze ii. blocking by prior tenotomy. Brain Research 449(1-2): 150-156

The conditioning lesion effects refer to the earlier formation and the accelerated regenration of axonal sprouts following two successive axotomines. In a previous study, we observed that a prior freeze or a prior cut of rat sciatic nerve resulted in differences in the enhancement of the regeneration rate and the reduction of the initial delay. These differences were interpreted as possible non-neuronal cells influence the intrinsic regulation of the conditioning lesion phenomenon. In the present study, we attempted to modify the status of the muscles using tenotomy before the prior nerve injury to determine the respective influence of the muscular cells on conditioning lesion effects. Thus, the conditioning lesion, which was either a cut or a freeze of the tibial nerve at the ankle, was performed 14 days after foot sole muscles were tenotomized, close to their insertion into the calcaneus bone. The test lesion was always a freeze of the sciatic nerve at midthigh performed 7 days following the prior lesion. The elongation of the regenerating sprouts was electrophysiologically evaluated and the regeneration rate as well as the initial delay were calculated by means of regression analysis. Tenotomy did not influence the regeneration as was demonstrated in a group with a single sciatic nerve lesion. In contrast, when prior lesion was performed, the tenotomy prevented both the enhancement of the rate of regeneration and the reduction of the initial delay, whatever was the type of the conditioning lesion. Since tenotomy is known to reduce protein synthesis in muscular cells, the ability of the tenotomized muscles to maintain a supply of trophic survival factors to the motor neuron could be reduced. On the other hand, if the conditioning lesion effects require some denervation-induced muscular factors promoting axonal outgrowth, their amount following tenotomy would be lesser. In both cases, subsequent axotomy would fail to elicit normal cell body response, therefore preventing the conditioning lesion effects.

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