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Enhancing KCNQ Channel Activity Improves Neurobehavioral Recovery after Spinal Cord Injury.
J Pharmacol Exp Ther
April 2020
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland (Z.W.); Department of Integrative Biology and Pharmacology, McGovern Medical School at UT Health, Houston, Texas (L.L., F.X.); Department of Critical Medicine, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China (F.X.); and Department of Neuroscience, Cell Biology and Anatomy at University of Texas Medical Branch, Galveston, Texas (G.X., D.D., Q.Y.)
Spinal cord injury (SCI) usually leads to acute neuronal death and delayed secondary degeneration, resulting in sensory dysfunction, paralysis, and chronic pain. Excessive excitation is one of the critical factors leading to secondary neural damage initiated by various insults. KCNQ/Kv7 channels are highly expressed in spinal neurons and axons and play an important role in controlling their excitability.
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