Dorsal root potentials and afferent input to the spinal cord in rats with an experimental peripheral neuropathy.

Compound action potentials (CAPs), dorsal root potentials (DRPs) and cord dorsum potentials evoked by stimulating the sciatic nerves have been measured in 4 control rats and in 19 rats with a constriction injury of one sciatic nerve produced by loose ligation of the nerve at mid-thigh level 5 days (n = 8) or 10 days (n = 11) before the acute experiments. The contralateral nerve was exposed but not ligated in a sham procedure. In all cases, the nerve was stimulated proximal to the lesion. At 5 days post-operative (PO) the maximal A-fibre CAPs on the nerve-injured side were not significantly different from those on the sham-operated side. At 10 days PO all animals showed a decrease in the CAP on the nerve-injured side. The mean CAP area on the nerve-injured side was 74.0% +/- 4.2 of the sham-operated side, which was significantly different (P less than 0.005). The sciatic nerves and L5 dorsal roots from 4 of the 10 day PO animals were examined histologically and showed no signs of demyelination or degeneration. The amplitude and area of the maximal DRPs were significantly smaller on the nerve-injured side than on the sham-operated side in all of the nerve-injured animals (P less than 0.01 at 5 days PO; P less than 0.05 at 10 days PO). The mean area of DRPs from the nerve-injured side was 61.7% +/- 10.1 and 46.8% +/- 7.5 of the DRPs from the sham-operated side in the 5 and 10 day PO animals, respectively. The DRPs evoked by sub-maximal afferent volleys were also measured. In all of the nerve-injured animals the CAP-DRP curve on the nerve-injured side was shifted to the right compared to that of the sham-operated side, such that a given size of CAP evoked a smaller DRP on the nerve-injured side than on the sham-operated side. We conclude that the constriction injury produces a decrease in the DRP generated by a volley in the injured nerve and that this change is independent of the decrease in the CAP seen in the injured nerve. We propose that the constriction injury affects the central mechanism responsible for generating primary afferent depolarization (PAD), and thus the pre-synaptic inhibitory control of the afferent input from the injured nerve is impaired.