All peroneal motoneurons of the rat survive crush injury but some fail to reinnervate their original targets

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Abstract
This is a quantitative study of the motoneuronal population of the rat's common peroneal nerve following severe crush injury of the sciatic nerve or its component branches. The crush was performed unilaterally under anesthesia for 60 seconds with hemostat jaws covered with tubing to form a smooth, 2 mm long, injured zone. Recovery from injury was allowed for 14 to 188 days. It was measured behaviorally using the sciatic functional index (SFI) and electrophysiologically by comparing the conduction velocity and amplitudes of evoked muscle action potentials prior to injury, and again after injury just before the nerve was labeled with horseradish peroxidase (HRP), and/or its wheat germ agglutinin conjugate (WGA‐HRP), 48–72 hours before sacrifice. The motoneurons were retrogradely labeled on both sides so that the uninjured side might serve as a control. On the injured side the nerves were labeled either distal or proximal to the crush site, The tibialis anterior muscles on both sides were removed and weighed. Spinal segments L2 to L6 were cut in serial, frozen cross‐sections. HRP reaction products were formed using TMB as the chromogen. The normal peroneal nerve was found to contain 634 ± 26 motoneurons (22 cases). The number of motoneurons labeled 5–15 mm distal to the injury site (22 cases) was 535 ± 69 or 84.4% of normal. In 12 cases in which the nerve was labeled 5 mm proximal to the injury normal population numbers (648 ± 30) were found. These counts demonstrated that the unlabeled 15.6% in the distal labeled cases had not vanished as a result of cell death. Instead, the unlabeled group was composed mainly of small motoneurons whose axons probably had not regenerated distal to the crushed zone. Mean soma size of injured neurons increased to maximum 3–6 weeks after injury and then gradually decreased in size over the following weeks to nearly normal values. This transient increase in size was due to two factors: (1) soma swelling in response to axonal injury, and (2) absence of many small motoneurons, presumably γ‐motoneurons, which were either incapable of, or prevented from, regenerating beyond the injury zone long after larger motoneurons had reinnervated their targets. SFI scores, muscle weights, and amplitude ratios of evoked potentials recovered to control values by 70–80 days post‐injury. Conduction velocities remained 20–25% below normal at the end of 80 days. These data suggest that because all motoneurons survived injury, it is possible for all of them to reinnervate their original targets under certain conditions providing that proper pathguides are available.