CONTRIBUTIONS OF INJURED AND INTACT AFFERENTS TO NEUROPATHIC PAIN IN AN EXPERIMENTAL RAT MODEL

Citation
Yw. Yoon et al., CONTRIBUTIONS OF INJURED AND INTACT AFFERENTS TO NEUROPATHIC PAIN IN AN EXPERIMENTAL RAT MODEL, Pain, 64(1), 1996, pp. 27-36
Citations number
50
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
PainACNP
ISSN journal
03043959
Volume
64
Issue
1
Year of publication
1996
Pages
27 - 36
Database
ISI
SICI code
0304-3959(1996)64:1<27:COIAIA>2.0.ZU;2-V
Abstract
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.