Changes in gene expression and neuronal phenotype in brain stem pain modulatory circuitry after inflammation
Changes in gene expression and neuronal phenotype in brain stem pain modulatory circuitry after inflammation
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DOI：
10.1152/jn.00534.2001
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发表时间：
2002-02-01
影响因子：
2.5
通讯作者：
Ren, K
中科院分区：
文献类型：
--
作者：
Miki, K;Zhou, QQ;Ren, K
最近的研究表明，下行性疼痛调节通路在炎症后经历了兴奋性的时间依赖性变化，包括易化和抑制。这些现象的细胞和分子机制尚不清楚。在本研究中，我们研究了N-甲基-D-天冬氨酸（NMDA）受体基因的表达和神经元的活动在延髓头端腹内侧（RVM），一个关键的结构，在疼痛调制电路，完全弗氏佐剂（CFA）诱导后爪炎症。逆转录聚合酶链反应分析表明，有上调编码NMDA受体亚基的mRNA在RVM炎症后。NR 1、NR 2A和NR 2B受体mRNA在炎症后5 h开始升高，持续1-7 d（P < 0.05-0.001），14 d恢复到对照组水平。Western blot分析表明，NR 2A亚基的蛋白质翻译产物也增加（P
Recent studies indicate that descending pain modulatory pathways undergo time-dependent changes in excitability following inflammation involving both facilitation and inhibition. The cellular and molecular mechanisms of these phenomena are unclear. In the present study, we examined N-methyl-D-aspartate (NMDA) receptor gene expression and neuronal activity in the rostral ventromedial medulla (RVM), a pivotal structure in pain modulatory circuitry, after complete Freund's adjuvant (CFA)-induced hindpaw inflammation. The reverse transcription polymerase chain reaction analysis indicated that there was an upregulation of mRNAs encoding NMDA receptor subunits in the RVM after inflammation. The increase in the NR1, NR2A, and NR2B receptor mRNAs started at 5 h, maintained for 1-7 days (P < 0.05-0.001) and returned to the control level at 14 days after inflammation. Western blot analysis indicated that the protein translation products of the NR2A subunit were also increased (P