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The following hypotheses were examined: 1. Rapid initial elongation of the regenerating axons in crushed nerves observed even in the absence of distal cell support is later slowed down or stops altogether. 2. If, in addition, Schwann cell proliferation in the proximal nerve stump is prevented, the reduction of the axon elongation rate during the prolonged absence of cell support beco­mes more severe. 3. Prior collateral sprouting which exposes neurons to higher NGF concentrations has a sti­mulatory effect on axon regeneration in the absence of cell support, therefore the axon regeneration rate is less affected. The rapid initial rate of sensory axon growth through acellular distal nerve segments decrea­ses 8 days after axonotmesis. During the next three weeks, retraction of leading axons towards the site of the lesion occurs and the number of axons distal to the crush site is reduced. Axon growth is resumed thereafter, but at a much lower rate. Mitomycin application, which pre­vents Schwann cell proliferation in the proximal stump, does not prevent the initial rapid axon elongation in the absence of cell support, but later the axons retract all the way to the crush site and no further growth occurs over 6 weeks. Exposure of regenerating axons to NGF during collateral sprouting enhances the initial elongation rate in the absence of cell sup­port, delays cessation of growth and prevents axon retraction. The number of axons distal to the lesion site remains high. Schwann cells in the distal nerve segment provide and maintain a favourable growth sub­stratum for regenerating axons during a prolonged time period after nerve injury. Growth promoting substances secreted by Schwann cells seem to enable elongation or prevent retrac­tion of axons even in the case of deterioration of the growth substratum. In the presence of good growth substratum, these substances moderately enhance the elongation rate of rege­nerating sensory axons.