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Chronic neuropathic pain–like behavior and brain‐borne IL‐1β
Author(s) -
del Rey Adriana,
Apkarian A. Vania,
Martina Marco,
Besedovsky Hugo O.
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2012.06621.x
Subject(s) - neuropathic pain , brainstem , neuroscience , nociception , hippocampal formation , spinal cord , prefrontal cortex , hippocampus , neuralgia , medicine , anesthesia , nerve injury , psychology , receptor , cognition
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.