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.
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.