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Spinal 5-HT3AR contributes to BmK I-induced inflammatory pain in rats

FU Jin, JIAO Yun-Lu, LI Zheng-Wei, JI Yong-Hua^*

Laboratory of Neuropharmacology and Neurotoxicology, Shanghai University, Shanghai 200444, China

Abstract

Subcutaneous injection of BmK I could be adopted to well establish a novel pain model. Moreover, 5-hydroxytryptamine (serotonin, 5-HT) receptor is involved in regulating animal pain-related behaviors. However, the underlying mechanism of 5-HT3R on BmK I-induced pain remains unclear. Animal behavioral testing, RT-PCR and Western blotting were used to yield the following results: first, intraplantar (i.pl.) injection of BmK I (10 μg) induced elevated mRNA and protein levels of 5-HT3AR in bilateral L4–L5 spinal cord; Second, intrathecal (i.t.) injection of ondansetron (a specific antagonist of 5-HT3AR) reduced spontaneous pain responses, attenuated unilateral thermal and bilateral mechanical hypersensitivity elicited by BmK I; Microglia could be activated by BmK I (i.pl.) in both sides of L4–L5 spinal cord, and this effect was reversed by intrathecal pre-treatment with 5-HT3AR antagonist. Meanwhile, the 5-HT3AR in L4–L5 spinal cord was almost co-localized with NeuN (a marker of nerve cell), but not co-expressed with Iba-1 (a marker of microglia). Finally, the expression level of CX3CL1 and CX3CR1 was reduced by intrathecal pre-treatment with ondansetron. Our results indicate that both 5-HT3AR signaling pathway and microglia are activated in the process of induction and maintenance of BmK I-induced pain nociception. Meanwhile, our results suggest that the neuronal 5-HT3AR may communicate with microglia indirectly via CX3CL1 which is involved in regulating the BmK I-induced hyperalgesia and sensitization.

Key words: BmK I-induced pain; 5-HT3AR; microglia; hyperalgesia and sensitization

Received: 2015-02-28　　Accepted: 2015-06-01

Corresponding author: 吉永华　　E-mail: yhji@staff.shu.edu.cn

Citing This Article：

FU Jin, JIAO Yun-Lu, LI Zheng-Wei, JI Yong-Hua. Spinal 5-HT3AR contributes to BmK I-induced inflammatory pain in rats. Acta Physiol Sin 2015; 67 (3): 283-294 (in Chinese with English abstract).