Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons

P. Honore, S. D. Rogers, M. J. Schwei, J. L. Salak-Johnson, N. M. Luger, M. C. Sabino, D. R. Clohisy, Patrick W Mantyh

Research output: Contribution to journalArticle

452 Citations (Scopus)

Abstract

The aim of this investigation was to determine whether murine models of inflammatory, neuropathic and cancer pain are each characterized by a unique set of neurochemical changes in the spinal cord and sensory neurons. All models were generated in C3H/HeJ mice and hyperalgesia and allodynia behaviorally characterized. A variety of neurochemical markers that have been implicated in the generation and maintenance of chronic pain were then examined in spinal cord and primary afferent neurons. Three days after injection of complete Freund's adjuvant into the hindpaw (a model of persistent inflammatory pain) increases in substance P, calcitonin gene- related peptide, protein kinase Cγ, and substance P receptor were observed in the spinal cord. Following sciatic nerve transection or L5 spinal nerve ligation (a model of persistent neuropathic pain) significant decreases in substance P and calcitonin gene-related peptide and increases in galanin and neuropeptide Y were observed in both primary afferent neurons and the spinal cord. In contrast, in a model of cancer pain induced by injection of osteolytic sarcoma cells into the femur, there were no detectable changes in any of these markers in either primary afferent neurons or the spinal cord. However, in this cancer-pain model, changes including massive astrocyte hypertrophy without neuronal loss, increase in the neuronal expression of c- Fos, and increase in the number of dynorphin-immunoreactive neurons were observed in the spinal cord, ipsilateral to the limb with cancer. These results indicate that a unique set of neurochemical changes occur with inflammatory, neuropathic and cancer pain in C3H/HeJ mice and further suggest that cancer induces a unique persistent pain state. Determining whether these neurochemical changes are involved in the generation and maintenance of each type of persistent pain may provide insight into the mechanisms that underlie each of these pain states. (C) 2000 IBRO.

Original languageEnglish (US)
Pages (from-to)585-598
Number of pages14
JournalNeuroscience
Volume98
Issue number3
DOIs
StatePublished - Jun 2000
Externally publishedYes

Fingerprint

Neuralgia
Sensory Receptor Cells
Spinal Cord
Afferent Neurons
Pain
Inbred C3H Mouse
Calcitonin Gene-Related Peptide
Hyperalgesia
Substance P
Maintenance
Neurokinin-1 Receptors
Galanin
Dynorphins
Spinal Nerves
Injections
Freund's Adjuvant
Neuropeptide Y
Sciatic Nerve
Chronic Pain
Astrocytes

Keywords

  • Astrocyte hypertrophy
  • Bone
  • c-Fos protein
  • Dynorphin
  • Osteolysis
  • Persistent pain

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons. / Honore, P.; Rogers, S. D.; Schwei, M. J.; Salak-Johnson, J. L.; Luger, N. M.; Sabino, M. C.; Clohisy, D. R.; Mantyh, Patrick W.

In: Neuroscience, Vol. 98, No. 3, 06.2000, p. 585-598.

Research output: Contribution to journalArticle

Honore, P. ; Rogers, S. D. ; Schwei, M. J. ; Salak-Johnson, J. L. ; Luger, N. M. ; Sabino, M. C. ; Clohisy, D. R. ; Mantyh, Patrick W. / Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons. In: Neuroscience. 2000 ; Vol. 98, No. 3. pp. 585-598.
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