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

H. Sun, K. Ren, C. M. Zhong, M. H. Ossipov, T. P. Malan, J. Lai, Frank Porreca

Research output: Contribution to journalArticle

101 Citations (Scopus)

Abstract

Peripheral nerve injury produces signs of neuropathic pain including tactile allodynia and thermal hyperalgesia, sensory modalities which may be associated with different neuronal pathways. Studies of spinally-transected, nerve-injured rats have led to suggestions that thermal hyperalgesia may be mediated 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 was explored using selective spinal lesions. Male Sprague-Dawley rats received L5/L6 spinal nerve ligation (SNL) and ipsilateral or contralateral (relative to the SNL side) lesions including spinal hemisections and bilateral and unilateral dorsal column lesions. The rats were maintained in a sling and monitored for tactile allodynia by measuring withdrawal thresholds to probing with von Frey filaments 24 h after the hemisection. Rats receiving dorsal column lesions demonstrated no motor deficits while rats receiving spinal hemisection showed paralysis of the paw which nevertheless responded to strong noxious stimulation. Spinal hemisection ipsilateral, but not contralateral, to SNL completely abolished tactile allodynia while maintaining spinal 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 ipsilateral to SNL also blocked tactile allodynia, but did not alter thermal hyperalgesia in SNL rats or increase thermal nociceptive responses in sham-operated rats. Lidocaine microinjected into the contralateral nucleus gracilis produced no changes in responses to tactile or thermal stimuli in either group. These results indicate that tactile allodynia after peripheral nerve injury is dependent upon inputs to supraspinal sites. Furthermore, it is apparent that afferent signals interpreted as tactile allodynia course through the ipsilateral dorsal columns and are relayed through the nucleus gracilis. This neuronal pathway is consistent with the interpretation that tactile allodynia pursuant to peripheral nerve injury is transmitted to the central nervous system by means of large diameter, myelinated fibers.

Original languageEnglish (US)
Pages (from-to)105-111
Number of pages7
JournalPain
Volume90
Issue number1-2
DOIs
StatePublished - Feb 1 2001

Fingerprint

Hyperalgesia
Spine
Wounds and Injuries
Spinal Nerves
Ligation
Peripheral Nerve Injuries
Lidocaine
Hot Temperature
Touch
Neuralgia
Paralysis
Sprague Dawley Rats
Reflex

Keywords

  • Ascending spinal dorsal column projections
  • Nerve injury
  • Tactile allodynia

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health
  • Neurology
  • Neuroscience(all)
  • Pharmacology
  • Clinical Psychology

Cite this

Nerve injury-induced tactile allodynia is mediated via ascending spinal dorsal column projections. / Sun, H.; Ren, K.; Zhong, C. M.; Ossipov, M. H.; Malan, T. P.; Lai, J.; Porreca, Frank.

In: Pain, Vol. 90, No. 1-2, 01.02.2001, p. 105-111.

Research output: Contribution to journalArticle

Sun, H. ; Ren, K. ; Zhong, C. M. ; Ossipov, M. H. ; Malan, T. P. ; Lai, J. ; Porreca, Frank. / Nerve injury-induced tactile allodynia is mediated via ascending spinal dorsal column projections. In: Pain. 2001 ; Vol. 90, No. 1-2. pp. 105-111.
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