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However, the mechanisms of this extra\u2010territorial pain induction still remain unclear. Glia and cytokines are known to facilitate perception of noxious input, raising a possibility that these non\u2010neuronal elements are involved in the induction and spread of allodynia\/hyperalgesia at non\u2010injured skin territory. One day after MN transection, tactile allodynia\/hyperalgesia developed on the ipsilateral WP area, which is in the non\u2010injured skin territory. The tactile allodynia\/hyperalgesia lasted for more than 56 days. In response to MN transection, astrocytes and microglia appeared to be in an activated state, and interleukin (IL)\u20101beta was up\u2010regulated in astrocytes in the trigeminal subnucleus caudalis (Vc). Allodynia\/hyperalgesia at WP area induced by MN transection was attenuated dose\u2010dependently by IL\u20101 receptor antagonist IL\u20101ra (i.t., 0.05, 0.5, and 5pg\/rat). Fos\u2010like immunoreactive (Fos\u2010Li) neurons were observed in the Vc after non\u2010noxious mechanical stimulation of the WP area in the rats with MN transection. Administration of IL\u20101ra also attenuated the number of Fos\u2010Li neurons dose\u2010dependently. Administration of a noncompetitive antagonist of NMDA receptors MK\u2010801 (i.t., 5\u03bcg\/rat) reversed allodynia\/hyperalgesia. IL\u20101 receptor type I (IL\u20101RI) was localized in Fos\u2010 and phospho NR1\u2010immunoreactive neurons. These results suggest that IL\u20101beta in the Vc plays an important role in the development of extra\u2010territorial tactile allodynia\/hyperalgesia after MN transection.<\/jats:p>","DOI":"10.1016\/j.ejpain.2010.10.006","type":"journal-article","created":{"date-parts":[[2010,11,20]],"date-time":"2010-11-20T09:36:18Z","timestamp":1290245778000},"source":"Crossref","is-referenced-by-count":7,"title":["IL\u20101beta in the trigeminal subnucleus caudalis contributes to extra\u2010territorial allodynia\/hyperalgesia following a trigeminal nerve 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