Accumulating evidence has demonstrated that the sodium-potassium-chloride co-transporter 1 (NKCC1) and potassium-chloride co-transporter 2 (KCC2) have a role in the modulation of pain transmission at the spinal level through chloride regulation in the pain pathway and by effecting neuronal excitability and pain sensitization. Dr. Yanbing He Zhujiang Hospital, Southern Medical University, China and his team found that intrathecal bumetanide could increase NKCC1 expression and decrease KCC2 expression in spinal cord neurons of rats with incisional pain. The authors presumed that intrathecal bumetanide has analgesic effects on incisional pain through inhibition of NKCC1. This paper was published in Neural Regeneration Research (Vol. 9, No. 10, 2014).
Article: " Analgesic effect of intrathecal bumetanide is accompanied by changes in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain," by Yanbing He1, 2, Shiyuan Xu1, Junjie Huang2, Qingjuan Gong2 (1 Department of Anesthesiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China; 2 Department of Anesthesiology and Pain Medicine, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China)
He YB, Xu SY, Huang JJ, Gong QJ. Analgesic effect of intrathecal bumetanide is accompanied by changes in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain. Neural Regen Res. 2014;9(10):1055-1062.
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