Growth of regenerating axons after peripheral nerve injury is determined predominantly by the micro-environment in the nerve segment distally to the lesion site. It is still contrversial as to what extent the proliferating Schwann cells (SC) in the distal stump support axon growth. If a frozen nerve graft containing basal laminae (BL) but not SCs was sutured to the proximal stump after nerve transection, the outgrowth of regenerating axons was slow and proceeded in parallel with the SC migrating from the proximal nenre stump.On the other hand, regenerating axons were able to grow fairly rapidly into the acellular distal nerve segment after crush injury, which leaves the BL tubes undamaged. The aim of the present work was to determine the role of cell support in the distal nerve stump on sensory axon regeneration after peripheral nerve injury. We hypothesized thatČ 1) Recovery of nociception in the skin after peripheral nerve crush is delayed but not prevented by short-term deprivation of cell support in the distal stump. 2) The rate of elongation of regenerating sensory axons after the nerve crush is greatly decreased by long-term deprivation of cellular support in distal nerve stump. In parallel the possibility that prior exposure of sensory neurons to high levels of NGF during collateral sprouting into denervated skin migh compensatefor the loss of cell support during subsequent injury and regeneration. Therefore, branches of the rat sciatic nerve were crushed and the nerve segment distally to the lesion site was frozen and thawed to eliminate SC, but leave their BL undamaged. The recovery of nociception in therats hind paw was tested by skin pinch test. The elongation rate of sensoryaxons regenerating in the absence of cellular support in the long segment of the distal stump was examined by the nerve pinch test and axon counting. (Abstract truncated at 2000 characters).

Muscle regeneration represents a short repetition of ontogenetic development from the myogenic stem cells to the innervated muscle fibers and can be used as a suitable experimental model to study biochemical characteristics of developing muscle cells. Therefore, ability to regulate acetylcholinesterase (AChE) either in absence or presence of innervation and ability of noninnervated muscle cells to form postsynaptic-apparatus-like sarcolemmal specializations was explored in regenerating muscles. Patterns and distribution of AChE molecular forms were studied in regenerating fast extensor digitorum longus (EDL) and slow soleus (SOL) muscle after ischaemic-toxic injury. AChE molecular forrns were analysed by velocity sedimentation in linear sucrose gradients. Histochemical and cytochemical methods were used to study localization and ultrastructure of focal accumulations of AChE in regenerating muscles. The extent of congruity with two other synaptic molecules, acetylcholine receptor (AChR) and Dolichos biflorus agglutinin binding glycoprotein (DBAR), was investigated. The patterns of AChE molecular forms in normal mature SOL and EDL muscles differ signifficantly, but no such differences were observed early in noninnerevated regenerating SOL and EDL muscles. All major AChE molecular forms were present in 8-day old noninnervated regenerating muscles. The 4S (G1) form predominatedbut the asymmetric A12 AChE molecular form contributed about 20 per cent of AChE activity. The activity of the lOS (G4) molecular form became predominant with increasing muscle maturation. These re sults show that immature regenerating myot from motor nerves. We assume that the satellite cells which gave rise to the regenerating myotubes originate from the late myoblasts and preserve their potential to synthesize the asymmetric AChE forms, inspite of long standstill and several divisions during regeneration.(abstract truncated at 2000 characters).