This study was conducted to determine the contribution of peripheral i
nputs from injured and intact afferent fibers to behavioral signs of n
europathic pain, using a previously developed neuropathic rat model. N
europathic injury was produced by tightly ligating the left L5 and L6
spinal nerves; this procedure induced rats to display neuropathic pain
behaviors in the ipsilateral hindlimb. The behaviors included signs o
f mechanical and cold allodynia, as well as ongoing pain. Five days af
ter neuropathic injury, peripheral inputs from injured segments (L5 an
d L6) or intact segments (L3 and L4) were blocked by either transectio
n of the dorsal roots or application of a local anesthetic (bupivacain
e) to the roots. Dorsal rhizotomy of the injured segments reduced all
components of neuropathic pain behaviors. In contrast, dorsal rhizotom
y of the uninjured segments abolished behavioral signs of mechanical a
nd cold allodynia, but signs of ongoing pain were preserved, Blocking
afferent inputs by application of bupivacaine mimicked the results of
dorsal rhizotomy, in a reversible manner. These results suggest that a
fferent signals from injured and intact fibers play distinctively diff
erent roles in neuropathic pain: inputs from injured afferents maintai
n all components of neuropathic pain, while those from intact afferent
s mediate evoked pain such as mechanical and cold allodynia. An hypoth
esis is proposed to explain the results of the present as well as othe
r published studies.