• Biochem. Biophys. Res. Commun. · Oct 2013

    Microglial activation of p38 contributes to scorpion envenomation-induced hyperalgesia.

    • Qing-Shan Niu, Feng Jiang, Li-Ming Hua, Jin Fu, Yun-Lu Jiao, Yong-Hua Ji, and Gang Ding.
    • Lab of Neuropharmacology and Neurotoxicology, Shanghai University, Shanghai 200444, PR China.
    • Biochem. Biophys. Res. Commun. 2013 Oct 25; 440 (3): 374-80.

    AbstractIntraplantar (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.Copyright © 2013 Elsevier Inc. All rights reserved.

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