Chronic neuropathic pain-like behavior and brain-borne IL-1β

Adriana del Rey*, Apkar Apkarian, Marco Martina, Hugo O. Besedovsky

*Corresponding author for this work

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Neuropathic pain in animals results in increased IL-1β expression in the damaged nerve, the dorsal root ganglia, and the spinal cord. Here, we discuss our results showing that this cytokine is also overexpressed at supraspinal brain regions, in particular in the contralateral side of the hippocampus and prefrontal cortex and in the brainstem, in rats with neuropathic pain-like behavior. We show that neuropathic pain degree and development depend on the specific nerve injury model and rat strain studied, and that there is a correlation between hippocampal IL-1β expression and tactile sensitivity. Furthermore, the correlations between hippocampal IL-1β and IL-1ra or IL-6 observed in control animals, are disrupted in rats with increased pain sensitivity. The lateralization of increased cytokine expression indicates that this alteration may reflect nociception. The potential functional consequences of increased IL-1β expression in the brain during neuropathic pain are discussed.

Original languageEnglish (US)
Pages (from-to)101-107
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1262
Issue number1
DOIs
StatePublished - Jan 1 2012

Fingerprint

Neuralgia
Interleukin-1
Chronic Pain
Brain
Rats
Animals
Cytokines
Interleukin 1 Receptor Antagonist Protein
Nociception
Touch
Spinal Ganglia
Prefrontal Cortex
Brain Stem
Interleukin-6
Hippocampus
Spinal Cord
Pain
Wounds and Injuries
Rat
Nerve

Keywords

  • Chronic pain
  • Hippocampus
  • Interleukin-1
  • Lateralization

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

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Chronic neuropathic pain-like behavior and brain-borne IL-1β. / del Rey, Adriana; Apkarian, Apkar; Martina, Marco; Besedovsky, Hugo O.

In: Annals of the New York Academy of Sciences, Vol. 1262, No. 1, 01.01.2012, p. 101-107.

Research output: Contribution to journalArticle

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