Abstract

The responses to injury of myelinated central axons in neonatal (5-day) and weanling (30-day) rats were compared, using the trochlear nerve fibres in the anterior medullary velum (AMV) as an experimental system. In intact animals, fibres of the trochlear nerve decussate completely in the AMV, to enter the contralateral nerve. Sprouting from proximal axon stumps was seen within 36 h after injury in silver-stained, whole mounts of mid-sagittally lesioned AMVs from weanlings. Subsequent growth produced a tangled axon mass which persisted until 15-20 days post-lesion (d.p.l.) but then began to degenerate. By 50 d.p.l., the majority of surviving axons looped within the AMV to enter the ipsilateral trochlear nerve; few axons remained growing randomly within the AMV. Axonal debris persisted within the velum 50 d.p.l. In neonatal rats, lesioned trochlear axons initially developed axon sprouts, but then degenerated with rapid clearance of debris, leaving the AMV devoid of both axons and degeneration products by 6 d.p.l. From 8 d.p.l., the velum became repopulated by axons which either grew randomly or looped to enter the ipsilateral peripheral nerve. Both patterns of axon growth were still observed 50 d.p.l. In both experimental groups, horseradish peroxidase injection to the right superior oblique muscle 40 d.p.l. indicated that at least some of the looping fibres observed within the lesioned AMVs originated in the ipsilateral trochlear nucleus. The origin of those axons growing randomly within the AMVs of neonatally-lesioned animals is unknown. The results are discussed with reference to current ideas concerning regeneration-inhibiting elements in the CNS, and regeneration-promoting factors in the PNS.

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