Selective loss of spinal GABAergic or glycinergic neurons is not necessary for development of thermal hyperalgesia in the chronic constriction injury model of neuropathic pain

E. Polgár, D. I. Hughes, J. S. Riddell, D. J. Maxwell, Z. Puskár, A. J. Todd

Research output: Contribution to journalArticle

157 Citations (Scopus)

Abstract

GABA and glycine are inhibitory neurotransmitters used by many neurons in the spinal dorsal horn, and intrathecal administration of GABAA and glycine receptor antagonists produces behavioural signs of allodynia, suggesting that these transmitters have an important role in spinal pain mechanisms. Several studies have described a substantial loss of GABA-immunoreactive neurons from the dorsal horn in nerve injury models, and it has been suggested that this may be associated with a loss of inhibition, which contributes to the behavioural signs of neuropathic pain. We have carried out a quantitative stereological analysis of the proportions of neurons in laminae I, II and III of the rat dorsal horn that show GABA- and/or glycine-immunoreactivity 2 weeks after nerve ligation in the chronic constriction injury (CCI) model, as well as in sham-operated and naïve animals. At this time, rats that had undergone CCI showed a significant reduction in the latency of withdrawal of the ipsilateral hindpaw to a radiant heat stimulus, suggesting that thermal hyperalgesia had developed. However, we did not observe any change in the proportion of neurons in laminae I-III of the ipsilateral dorsal horn that showed GABA- or glycine-immunoreactivity compared to the contralateral side in these animals, and these proportions did not differ significantly from those seen in sham-operated or naïve animals. In addition, we did not see any evidence for alterations of GABA- or glycine-immunostaining in the neuropil of laminae I-III in the animals that had undergone CCI. Our results suggest that significant loss of GABAergic or glycinergic neurons is not necessary for the development of thermal hyperalgesia in the CCI model of neuropathic pain.

Original languageEnglish
Pages (from-to)229-239
Number of pages11
JournalPain
Volume104
Issue number1-2
DOIs
Publication statusPublished - Jul 2003

Fingerprint

Hyperalgesia
Neuralgia
Constriction
Neurons
Wounds and Injuries
Glycine
gamma-Aminobutyric Acid
Glycine Receptors
GABA-A Receptor Antagonists
GABAergic Neurons
Neuropil
Spinal Cord Dorsal Horn
Ligation
Neurotransmitter Agents
Hot Temperature
Pain

Keywords

  • Disector method
  • GABA
  • Glycine
  • Immunocytochemistry
  • Post-embedding

ASJC Scopus subject areas

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

Cite this

Selective loss of spinal GABAergic or glycinergic neurons is not necessary for development of thermal hyperalgesia in the chronic constriction injury model of neuropathic pain. / Polgár, E.; Hughes, D. I.; Riddell, J. S.; Maxwell, D. J.; Puskár, Z.; Todd, A. J.

In: Pain, Vol. 104, No. 1-2, 07.2003, p. 229-239.

Research output: Contribution to journalArticle

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