Supraspinal involvement in the production of mechanical allodynia by spinal nerve injury in rats

Backil Sung, Heung Sik Na, Yang In Kim, Young Wook Yoon, Hee Chul Han, Sook Hyun Nahm, Seung Kil Hong

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

This study examined whether or not the production of mechanical allodynia in a rat model of neuropathic pain required an involvement of supraspinal site(s). To this aim, we assessed the effect of spinal cord section at the L1 segment level on the mechanical allodynia sign (i.e. tail flick/twitch response), which was elicited by innocuous von Frey hair stimulation of the tail after unilateral transection of the tail-innervating nerve superior caudal trunk (SCT) at the level between the S3 and S4 spinal nerves. Cord transection or hemisection of the cord ipsilateral to the injured SCT drastically (though not completely) blocked the behavioral sign of mechanical allodynia (leaving noxious pinprick-elicited tail withdrawal reflex intact), whereas sham section or contralateral hemisection of the cord was without effect. These results suggest that the generation of mechanical allodynia following partial peripheral nerve injury involves transmission of the triggering sensory signal to a site(s) rostral to the L1 segment via an ipsilateral pathway(s).

Original languageEnglish
Pages (from-to)117-119
Number of pages3
JournalNeuroscience Letters
Volume246
Issue number2
DOIs
Publication statusPublished - 1998 Apr 24

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Spinal Injuries
Spinal Nerves
Hyperalgesia
Tail
Peripheral Nerve Injuries
Neuralgia
Hair
Reflex
Spinal Cord

Keywords

  • Allodynia
  • Hyperalgesia
  • Nerve injury
  • Neuropathic pain
  • Spinal reflex

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Supraspinal involvement in the production of mechanical allodynia by spinal nerve injury in rats. / Sung, Backil; Na, Heung Sik; Kim, Yang In; Yoon, Young Wook; Han, Hee Chul; Nahm, Sook Hyun; Hong, Seung Kil.

In: Neuroscience Letters, Vol. 246, No. 2, 24.04.1998, p. 117-119.

Research output: Contribution to journalArticle

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