REINNERVATION OF RAT MUSCLES VIA VOLKENSIN-AFFECTED AND NORMAL PERIPHERAL-NERVE CONDUITS

Volkensin is a neurotoxic lectin which, when injected into a periphera l nerve is retrogradely transported to the cell body and causes it to die. Accordingly, volkensin-affected peripheral nerves rapidly degener ate. It is, however, not clear whether axonal growth can take place wi thin these degenerated nerves. In this study the ability of volkensin- treated and untreated degenerated peripheral nerves to support regener ation 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 prox imal stump of the deep tibial nerve was connected to the distal sectio n of the cut, thus giving a volkensin-treated peroneal nerve. In the t hird group, 10 days after the peroneal nerve was treated with volkensi n, the proximal stump of the deep tibial nerve was connected directly to the extensor digitorum longus (EDL) muscle. In Group 4 the volkensi n-treated peroneal nerve was left intact. Six weeks after surgical int ervention 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 max imal tetanic tension produced by the contralateral EDL muscle. Signifi cantly less recovery of function was achieved by EDL muscles in Group 2 animals (9.3 +/- 2.5%). Muscles from Group 3, where the healthy nerv e 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 Sc hwann cells was observed in the muscles from Groups 1 and 3, but not i n Group 2. Thus, volkensin-treated peripheral nerves provide a poor co nduit for regenerating nerve fibres though muscles denervated, by trea tment with volkensin, and can accept reinnervation by healthy nerves. The possible mechanisms that render the volkensin treated peripheral s tump a poor conduit for healthy axons is discussed. (C) 1997 Elsevier Science Ireland Ltd.