Journal of Neuroscience, Vol 14, 2659-2673, Copyright © 1994 by Society for Neuroscience
Early peripheral nerve regeneration after crushing, sectioning, and freeze studied by implanted electrodes in the cat
K Fugleholm, H Schmalbruch and C Krarup
Institute of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
Regeneration of axons after Wallerian degeneration is influenced by various
factors localized to the distal nerve stump. We have examined elongation of
axons to assess the relative influence of basal lamina and of Schwann cells
in lesions with and without interruption of the Schwann cell tubes. In
particular, we wanted to follow the growth of axons throughout the same
distal nerve stump. Silicone cuff and patch electrodes with multiple
contacts were therefore implanted around hindlimb nerves proximal and
distal to the lesion. The tibial nerve was cut and sutured (15 nerves) or
crushed (10 nerves). A 20-25-mm-long segment distal to the lesion was in
addition frozen in four crushed and in seven sectioned nerves to eliminate
the Schwann cells. Six unlesioned tibial nerves from four cats served as
control. Reinnervation of plantar muscle occurred 42-54 d after nerve
crushing and 42-84 d after nerve sectioning (P < 0.01). Regeneration was
followed by weekly electrophysiological observations that allowed serial
identification of the fastest-growing individual axons, with conduction
velocities of 0.5-3 m/sec and amplitudes of 0.15-0.5 microV. Unmyelinated
axons were present at the most distal lead of the electrode array from
which action potentials were identified. The rate of elongation after both
crushing and crush+freeze was 3-4 mm/d, and after sectioning only 2.5 mm/d
(P < 0.01). Freezing in addition to sectioning was associated with even
slower elongation of 1.2 mm/d. Distal to the frozen portion of the nerve
elongation accelerated. Our findings suggest that regeneration was slowed
throughout the nerve distal to a sectioning compared with a crushing
lesion, and that depletion of Schwann cells only influenced axonal
elongation after interruption of the basal lamina. This suggests that the
basal lamina tubes at the lesion site may facilitate the action of
neurotropic factors of distal origin.
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