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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

Poster presentation

Intermittent cold stress-induced experimental fibromyalgia model in mice - pharmacology and neurobiology

Kohei Araki*, Michiko Nishiyori and Hiroshi Ueda

  • * Corresponding author: Kohei Araki

Author affiliations

Division of Molecular Pharmacology and Neurosciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8521, Japan

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Citation and License

Arthritis Research & Therapy 2012, 14(Suppl 1):P6  doi:10.1186/ar3607


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/14/S1/P6


Published:9 February 2012

© 2012 Araki et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Poster presentation

Stress-induced pain, as in Fibromyalgia (FM), is considered to be caused by intense events involving physical and psychological injury and is reinforced by successive stress. Previously, we have established a novel mice model of FM, using intermittent cold stress (ICS) exposure. Mice given ICS caused abnormal pain, including mechanical allodynia and hyperalgesia to nociceptive thermal and chemical stimuli, which lasted for more than 2 weeks. In contrast, those given constant cold stress (CCS) did not. The abnormal pain was generalized, female-predominant and specific for A-delta and A-beta, but not C-fiber-stimuli in the electrical stimulation-induced nociceptive test. The mechanical allodynia induced by ICS was effectively suppressed by intraperitoneal or intracerebroventricular injection of gabapentin. The potency and duration of anti-allodynia effects were much higher and longer, respectively, than the neuropathic pain induced by sciatic nerve injury. Taken together, these findings indicate that mice given ICS manifest most of characteristics observed in fibromyalgia patients in terms of pharmacology and pain physiology.

Acknowledgements

The research described in this article was supported in part by MEXT KAKENHI (17109015 to Hiroshi Ueda) and Health Labor Sciences Research Grants from the Ministry of Health, Labor and Welfare of Japan (to Hiroshi Ueda): "Research on Allergic disease and Immunology" also supported this work.

References

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    Mol Pain 2008, 4:52. PubMed Abstract | BioMed Central Full Text | PubMed Central Full Text OpenURL

  2. Nishiyori M, Nagai J, Nakazawa T, Ueda H: Absence of morphine analgesia and its underlying descending serotonergic activation in an experimental mouse model of fibromyalgia.

    Neurosci Lett 2010, 472:184-187. PubMed Abstract | Publisher Full Text OpenURL