Ryu Ji-Won, Lee Jun-Hyuk, Choi Yung-Hyun, Lee Yong-Tae, Choi Byung-Tae
Department of Physiology, College of Oriental Medicine, Dong-Eui University, Busan 614-052, Republic of Korea.
Brain Res Bull. 2008 Mar 28;75(5):687-91. doi: 10.1016/j.brainresbull.2007.11.005. Epub 2007 Dec 3.
The present study investigated the role of inhibitor of protein phosphatases 1 and 2A on the modulation of the phosphorylation of the spinal N-methyl-D-aspartate receptor (NMDAR) NR1 and NR2B subunits following electroacupuncture (EA) stimulation in rats. Bilateral 2Hz EA stimulations with 1.0 mA were delivered at those acupoints corresponding to Zusanli and Sanyinjiao to men via needles for 30 min. EA analgesia was slightly reduced by the intrathecal injection of calyculin A during EA stimulation. At 60 min after the termination of EA stimulation, the levels of c-fos, serine phosphorylation of NR1 and NR2B by Western analysis had increased in the L(4-5) segments of the spinal cord after EA treatment. These expressions were enhanced by the intrathecal injection of calyculin A and immunohistochemical analyses confirmed the significant increase of these proteins. As for the regional reaction of NMDAR subunits, a mean integrated optical density of phosphorylated NR1 and NR2B subunits was potentiated by calyculin A injections in the superficial laminae and neck region and superficial laminae and nucleus proprius, respectively. It can be concluded that protein phosphatase may play an important role in EA analgesia by modulating the phosphorylation state of spinal NMDAR subunits.
本研究探讨了蛋白磷酸酶1和2A的抑制剂在大鼠电针(EA)刺激后对脊髓N-甲基-D-天冬氨酸受体(NMDAR)NR1和NR2B亚基磷酸化调节中的作用。通过针以1.0 mA的电流对对应于足三里和三阴交的穴位进行双侧2Hz的EA刺激,持续30分钟。在EA刺激期间鞘内注射花萼海绵诱癌素A会使EA镇痛作用稍有减弱。在EA刺激结束后60分钟,经蛋白质免疫印迹分析,EA处理后脊髓L(4 - 5)节段中c-fos、NR1和NR2B的丝氨酸磷酸化水平有所升高。鞘内注射花萼海绵诱癌素A可增强这些表达,免疫组织化学分析证实了这些蛋白质的显著增加。至于NMDAR亚基的区域反应,在浅表层和颈部区域以及浅表层和固有核分别注射花萼海绵诱癌素A后,磷酸化NR1和NR2B亚基的平均积分光密度增强。可以得出结论,蛋白磷酸酶可能通过调节脊髓NMDAR亚基的磷酸化状态在EA镇痛中发挥重要作用。