IL-10 and IL-1β mediate neuropathic-pain like behavior in the ventrolateral orbital cortex.

Abstract

Previous evidence has shown that the glial cells can be activated by peripheral nerve injury and release both pro-inflammatory and anti-inflammatory cytokines, which play crucial roles in the establishment and maintenance of neuropathic pain. The present study examined the roles of anti-inflammatory cytokine IL-10 and pro-inflammatory IL-1β on allodynia induced by spared nerve injury (SNI) in the ventrolateral orbital cortex (VLO) in the rat. The mechanical paw withdrawal threshold (PWT) was measured using von-Frey filaments. Microinjection of IL-10 (0.1, 0.5, 1 μg/0.5 μl) into the VLO, contralateral to the site of nerve injury attenuated allodynia; PWT increased in a dose-dependent manner. Similar to IL-10, administration of rabbit anti-rat IL-1β antibody (0.1, 1.0 and 10 ng/0.5 μl) into the same VLO site also alleviated allodynia with a dose-dependent fashion. Moreover, western blotting results showed expression levels of IL-10 and IL-1β significantly up-regulated in the contralateral VLO of SNI rats as compared with that of sham-operated rats. These results suggest that anti-inflammatory cytokine IL-10 and pro-inflammatory cytokine IL-1β mediate neuropathic-pain like behavior at the cerebral cortex level; IL-10 released from activated glial cells in the VLO can potentially attenuate allodynia while IL-1β released from activated glial cells in the VLO can potentially maintain or facilitate allodynia. These results provide new insights and site for therapy at the cerebral cortex level in neuropathic pain condition.