Electrophysiological evidence for hyperalgesia in the peripheral neuropathy.

A peripheral neuropathy was produced in adult rats by placing loosely constrained ligature around the common sciatic nerve. At the ligature region of the nerve, demyelination developed. The postoperative behavior of these rats indicated that hyperalgesia and allodynia were produced. The electrical activity pattern of the damaged fibers was remarkably different from those of normal nerves: there were some abnormal spontaneous afferent firings from the injured fibers; multi-impulse responses of C-fiber to single shock was recorded; a lasting firing was elicited after the injured region was gently pressed or by oil drops at 40 degrees C; an antidromic electric stimulus to the injured region, stimulations of L5 sympathetic ganglion or systemic administration of noradrenaline, all caused an increase in on-going spontaneous discharges of the injured fibers or brought the silent fibers into firing. Stimulation of the dorsal roots of the sciatic nerve produced no effect on their activities or caused a pause of the on-going discharges of them. Phentolamine, an alpha receptor blocker, ceased the abnormal firing, but did not affect the normal fiber firings. It is hypothesized that noradrenaline released by the sympathetic nerve would be an important factor responsible for both hyperalgesia and allodynia following injury of peripheral nerve.