Affiliations: Department of Ophthalmology, Albert Szent-Györgyi Medical University, P.O. Box 407, H-6701 Szeged, Hungary | Department of Anatomy and Developmental Biology, Centre for Neuroscience, University College London, London WC1E 6BT, UK
Abstract: Volkensin is a neurotoxic lectin which, when injected into a peripheral nerve is retrogradely transported to the cell body and causes it to die. Accordingly, volkensin-affected peripheral nerves rapidly degenerate. It is, however, not clear whether axonal growth can take place within these degenerated nerves. In this study the ability of volkensin-treated and untreated degenerated peripheral nerves to support regeneration of healthy axons was compared. Four groups of animals were used, in Group 1 the peroneal nerve was cut and 10 days later the proximal stump of the deep tibial nerve was sutured to the distal stump of the peroneal nerve (10 days after axotomy). In the second group of animals the peroneal nerve was treated with volkensin, 10 days later the proximal stump of the deep tibial nerve was connected to the distal section of the cut, thus giving a volkensin-treated peroneal nerve. In the third group, 10 days after the peroneal nerve was treated with volkensin, the proximal stump of the deep tibial nerve was connected directly to the extensor digitorum longus (EDL) muscle. In Group 4 the volkensin-treated peroneal nerve was left intact. Six weeks after surgical intervention the tension of both EDL muscles was recorded and the muscles were processed for histological visualisation of endplates and axons. EDL muscles from Group 1 animals produced 36.5 ± 11.3% S.E.M of maximal tetanic tension produced by the contralateral EDL muscle. Significantly less recovery of function was achieved by EDL muscles in Group 2 animals (9.3 ± 2.5%). Muscles from Group 3, where the healthy nerve was sutured directly into the EDL muscle that had been denervated by volkensin treatment had a significantly better recovery than Group 2 muscles (23 ± 3%). Sprouting of nerve fibres and proliferation of Schwann cells was observed in the muscles from Groups 1 and 3, but not in Group 2. Thus, volkensin-treated peripheral nerves provide a poor conduit for regenerating nerve fibres though muscles denervated, by treatment with volkensin, and can accept reinnervation by healthy nerves. The possible mechanisms that render the volkensin treated peripheral stump a poor conduit for healthy axons is discussed.
