Abnormal discharge originates at the site of nerve injury in experimental constriction neuropathy (CCI) in the rat.

Rats with an experimental painful peripheral neuropathy created by placing loosely constrictive ligatures around the sciatic nerve (the CCI model) display heat-hyperalgesia on the affected limb. Pain threshold was studied using the paw withdrawal method. Electrophysiological recording from myelinated primary afferent axons revealed spontaneous impulse activity which originated at the site of nerve constriction. Overall 10.1 +/- 1.5% of the fibers sampled had spontaneous activity during the period 2-14 days post injury. The spontaneous activity fell into three patterns: (1) 'tonic' rhythmic pattern, in which the interval between successive spikes in a train was uniform, ranging from 25-50 ms (discharge rate 20-40 Hz); (2) interrupted, bursty or 'on-off' pattern, with variable silent period between high frequency bursts; and (3) 'irregular' ongoing pattern with random inter-spike intervals (5-15 Hz). There was a correlation between the prevalence and pattern of spontaneous activity, and the development of hyperalgesia post-injury. Axons trapped at the injury site including ones with and without spontaneous activity, became hyperexcitable to mechanical stimulation. The location of mechanosensitive spots progressively shifted over the period 2-14 days from the proximal to the distal part of the injury site. The spontaneous discharge of injured primary afferent fibers may contribute to abnormal sensation in these animals.