Nerve injury-induced tactile allodynia is mediated via ascending spinal dorsal column projections

Citation
H. Sun et al., Nerve injury-induced tactile allodynia is mediated via ascending spinal dorsal column projections, PAIN, 90(1-2), 2001, pp. 105-111
Citations number
36
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
PAIN
ISSN journal
03043959 → ACNP
Volume
90
Issue
1-2
Year of publication
2001
Pages
105 - 111
Database
ISI
SICI code
0304-3959(20010201)90:1-2<105:NITAIM>2.0.ZU;2-V
Abstract
Peripheral nerve injury produces signs of neuropathic pain including tactil e allodynia and thermal hyperalgesia, sensory modalities which may be assoc iated with different neuronal pathways. Studies of spinally-transected, ner ve-injured rats have led to suggestions that thermal hyperalgesia may be me diated predominately through local spinal circuitry whereas ascending input to supraspinal sites is critical to the manifestation of tactile allodynia . Here, the nature of ascending spinal input mediating tactile allodynia wa s explored using selective spinal lesions. Male Sprague-Dawley rats receive d L-5/L-6 spinal nerve ligation (SNL) and ipsilateral or contralateral (rel ative to the SNL side) lesions including spinal hemisections and bilateral and unilateral dorsal column lesions. The rats were maintained in a sling a nd monitored for tactile allodynia by measuring withdrawal thresholds to pr obing with von Frey filaments 24 h after the hemisection. Rats receiving do rsal column lesions demonstrated no motor deficits while rats receiving spi nal hemisection showed paralysis of the paw which nevertheless responded to strong noxious stimulation Spinal hemisection ipsilateral, but not contral ateral, to SNL completely abolished tactile allodynia while maintaining spi nal nocifensive reflexes to noxious pinch. Bilateral and ipsilateral dorsal column lesions blocked tactile allodynia while contralateral dorsal column lesions did not. Administration of lidocaine into the nucleus gracilis ips ilateral to SNL also blocked tactile allodynia, but did not after thermal h yperalgesia in SNL rats or increase thermal nociceptive responses in sham-o perated rats. Lidocaine microinjected into the contralateral nucleus gracil is produced no changes in responses to tactile or thermal stimuli in either group. These results indicate that tactile allodynia after peripheral nerv e injury is dependent upon inputs to supraspinal sites. Furthermore, it is apparent that afferent signals interpreted as tactile allodynia course thro ugh the ipsilateral dorsal columns and are relayed through the nucleus grac ilis. This neuronal pathway is consistent with the interpretation that tact ile allodynia pursuant to peripheral nerve injury is transmitted to the cen tral nervous system by means of large diameter, myelinated fibers. (C) 2001 International Association for the Study of Pain. Published by Elsevier Sci ence B.V. All rights reserved.