TY - JOUR PY - 2013// TI - Microglial activation of p38 contributes to scorpion envenomation-induced hyperalgesia JO - Biochemical and biophysical research communications A1 - Niu, Qing-Shan A1 - Jiang, Feng A1 - Hua, Li-Ming A1 - Fu, Jin A1 - Jiao, Yun-Lu A1 - Ji, Yong-Hua A1 - Ding, Gang SP - 374 EP - 380 VL - 440 IS - 3 N2 - Intraplantar (i.pl.) injection of BmK I, a receptor site 3-specific modulator of voltage-gated sodium channels (VGSCs) from the venom of scorpion Buthus martensi Karsch (BMK), was shown to induce long-lasting and spontaneous nociceptive responses as demonstrated through experiments utilizing primary thermal and mirror-imaged mechanical hypersensitivity with different time course of development in rats. In this study, microglia was activated on both sides of L4-L5 spinal cord by i.pl. injection of BmK I. Meanwhile, the activation of p38/MAPK in L4-L5 spinal cord was found to be co-expressed with OX-42, the cell marker of microglia. The unilateral thermal and bilateral mechanical pain hypersensitivity of rat induced by BmK I was suppressed in a dose-dependent manner following pretreatment with SB203580 (a specific inhibitor of p-p38). Interestingly, microglia activity was also reduced in the presence of SB203580, which suggests that BmK I-induced microglial activation is mediated by p38/MAPK pathway. Combined with previously published literature, the results of this study demonstrate that p38-dependent microglial activation plays a role in scorpion envenomation-induced pain-related behaviors.
Language: en
LA - en SN - 0006-291X UR - http://dx.doi.org/10.1016/j.bbrc.2013.09.071 ID - ref1 ER -