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Journal Article

Citation

Niu QS, Jiang F, Hua LM, Fu J, Jiao YL, Ji YH, Ding G. Biochem. Biophys. Res. Commun. 2013; 440(3): 374-380.

Affiliation

Lab of Neuropharmacology and Neurotoxicology, Shanghai University, Shanghai 200444, P.R. China.

Copyright

(Copyright © 2013, Academic Press)

DOI

10.1016/j.bbrc.2013.09.071

PMID

24064352

Abstract

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

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