Axonal cross-excitation in nerve-end neuromas: Comparison of A- and C- fibers

1. We recorded from single afferent axons ending in chronic sciatic nerve end neuromas in rats with the use of the teased-fiber method. Axons were sought that had ongoing impulse discharge originating in the neuroma. 2. Recording from myelinated (A-) fibers, tetanic stimulation of neighboring axons (50 Hz, 5 or 10 s, intensity adequate to drive A-fibers) caused an increase, and sometimes a decrease, in the rate of ongoing discharge in 68% of the fibers tested. In addition, some initially silent neuroma A-fibers (1.4%) were activated in this way. Both Aβ and Aδ fibers responded, although the likelihood of response was greater in Aβ fibers. We call this form of interfiber cross-excitation 'crossed afterdischarge.' 3. In contrast to A-fibers, crossed afterdischarge was evoked with these stimulation parameters in ≤5% of the spontaneously active unmyelinated (C-) fibers sampled. No initially silent C-fibers were activated. 4. C-fibers remained largely insensitive to cross-excitation by neighboring axons even when the strength of stimulus pulses was increased so as to include neighboring A+C- fibers. 5. The difference between A- and C-fibers could not be accounted for on the basis of the maturity of the neuroma, rate and pattern of ongoing discharge, or use of Flaxedil paralysis. 6. The difference between A- and C- fibers is discussed in terms of two alternative mechanisms that may underlie crossed afterdischarge: mediation by a neurotransmitter(s) in a nonsynaptic mode, and mutual K⁺ depolarization. 7. It has been proposed that axonal cross-excitation contributes to the neuropathic paraesthesias and dysaesthesias often reported by patients with nerve injury. The finding that injured C-fibers are much less prone to cross-excitation than injured A- fibers constrains the possible role of this mechanism in postinjury neuropathic pain.