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Treadmill training enhances axon regeneration in injured mouse peripheral nerves without increased loss of topographic specificity
Author(s) -
English Arthur W.,
Cucoranu Delia,
Mulligan Amanda,
Sabatier Manning
Publication year - 2009
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.22149
Subject(s) - treadmill , sciatic nerve , axon , peripheral , regeneration (biology) , medicine , stimulation , tibial nerve , spinal cord , axoplasmic transport , anatomy , anesthesia , biology , microbiology and biotechnology , psychiatry
Abstract We investigated the extent of misdirection of regenerating axons when that regeneration was enhanced by using treadmill training. Retrograde fluorescent tracers were applied to the cut proximal stumps of the tibial and common fibular nerves 2 or 4 weeks after transection and surgical repair of the mouse sciatic nerve. The spatial locations of retrogradely labeled motoneurons were studied in untreated control mice and in mice receiving 2 weeks of treadmill training, according to either a continuous protocol (10 m/minute, 1 hour/day, 5 days/week) or an interval protocol (20 m/minute for 2 minutes, followed by a 5‐minute rest, repeated four times, 5 days/week). More retrogradely labeled motoneurons were found in both treadmill‐trained groups. The magnitude of this increase was as great as or greater than that found after using other enhancement strategies. In both treadmill‐trained groups, the proportions of motoneurons labeled from tracer applied to the common fibular nerve that were found in spinal cord locations reserved for tibial motoneurons in intact mice were no greater than in untreated control mice and significantly less than those found after electrical stimulation or chondroitinase treatment. Treadmill training in the first 2 weeks following peripheral nerve injury produces a marked enhancement of motor axon regeneration without increasing the propensity of those axons to choose pathways leading to functionally inappropriate targets. J. Comp. Neurol. 517:245–255, 2009. © 2009 Wiley‐Liss, Inc.