5-HT2-7受体亚型mRNAs在坐骨神经分支选择性损伤模型大鼠背根神经节的表达变化

TEMPORAL CHANGES OF THE EXPRESSION OF 5-HT_ ( 2～7) RECEPTOR mRNAs IN DORSAL ROOT GANGLIA INDUCED BY SPARED NERVE INJURY IN THE RAT

本研究利用反转录-聚合酶链式反应(RT-PCR)方法,观察了坐骨神经分支选择性损伤(SNI)所致神经病理性痛条件下,大鼠背根神经节(DRG)中5-HT2～7受体亚型mRNAs的时程表达变化.用RT-PCR方法在正常大鼠DRG中检测到5-HT2A、5-HT3、5-HT4、5-HT5A和5-HT7受体亚型mRNAs的表达,但未检测到5-HT2B、5-HT2c、5-HT5B和5-HT6受体亚型mRNAs.SNI能诱导5-HT2A、5-HT3、5-HT4和5-HT7受体亚型mRNAs在损伤侧DRG的表达上调.其中,5-HT2A受体亚型mRNA的表达在术后3 d时开始升高,持续增加至28 d;5-HT3受体亚型mRNA的表达在术后4 d时明显增加,14 d时达到高峰;5-HT4受体亚型mRNA于术后3 d的表达明显增加,21 d时达到高峰;5-HT7受体亚型mRNA的表达在术后1 d时即显著升高,一直维持高水平的表达至28 d.未检测到5-HT5A受体亚型mRNA的表达变化.在SNI对侧的DRG,各受体亚型mRNAs的表达未出现明显变化.部分5-HT受体亚型在SNI模型DRG的表达具有不同的时程变化特点,提示它们在SNI所致的神经病理性痛中发挥着不同的作用.

In the present study, reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the changes of the mRNAs expression of 5-HT_ 2～7 receptor subtypes in the rat dorsal root ganglia (DRG) induced by spared nerve injury (SNI). The present results showed that mRNAs of 5-HT_ 2A, 5-HT_3, 5-HT_4, 5-HT_ 5A and 5-HT_7 receptor subtypes were present in the DRG, whereas mRNAs of 5-HT_ 2B, 5-HT_ 2C, 5-HT_ 5B and 5-HT_6 receptor subtypes were absent. SNI resulted in increased expression of 5-HT_ 2A, 5-HT_3, 5-HT_4 and 5-HT_7 receptor subtypes mRNAs in the ipsilateral DRG, however, no such change was observed for 5-HT_ 5A receptor subtype mRNA. 5-HT_ 2A receptor subtype mRNA began to increase at 3 d after SNI and kept at increased level to 28 d. The expression of 5-HT_3 and 5-HT_4 receptor mRNAs significantly increased at 4 d and 3 d after SNI, reached a peak at 14 d and 21 d, respectively. SNI also resulted in a significant increase in the mRNA expression of 5-HT_7 receptor subtype at 1 d, then maintained at a high level to 28 d. In the DRGs contralateral to the SNI, no significant changes were observed for mRNAs of these receptor subtypes. The present studies revealed the different temporal expression pattern of 5-HT receptor subtypes mRNAs in rat DRG after SNI, suggesting that each 5-HT receptor subtype might play different roles in SNI induced neuropathic pain.