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World J Gastroenterol. 2016 Feb 7;22(5):1834-43. doi: 10.3748/wjg.v22.i5.1834.

Electroacupuncture at ST25 inhibits jejunal motility: Role of sympathetic pathways and TRPV1.

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Zhi Yu, Na Zhang, Chun-Xia Lu, Ting-Ting Pang, Kai-Yue Wang, Jing-Feng Jiang, Bin Xu, Key Laboratory of Integrated Acupuncture and Drugs, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu Province, China.



To investigate whether electroacupuncture (EA) at ST25 affects jejunal motility in vivo and if so, whether a sympathetic pathway is involved.


Jejunal motility was assessed using a manometric balloon placed in the jejunum approximately about 3-5 cm away from the suspensory ligament of the duodenum in anesthetized animals. The effects of EA at ST25 were measured in male Sprague-Dawley rats, some of which were treated with propranolol or clenbuterol (EA intensities: 1, 3, 5, 7, and 9 mA), and in male transient receptor potential vanilloid-1 (TRPV1) (capsaicin receptor) knockout mice (EA intensities: 1, 2, and 4 mA).


Anesthetized rats exhibited three types of fasting jejunal motor patterns (types A, B, and C), and only type C rats responded to EA stimulation. In type C rats, EA at ST25 significantly suppressed the motor activity of the jejunum in an intensity-dependent manner. The inhibitory effect of EA was weakened by propranolol (β adrenoceptor antagonist) and disappeared with clenbuterol (β adrenoceptor agonist) induced inhibition of motility, suggesting that the effect of EA on motility is mediated via a sympathetic pathway. Compared with wild-type mice, EA at ST25 was less effective in TRPV1 knockout mice, suggesting that this multi-modal sensor channel participates in the mechanism.


EA at ST25 was found to inhibit jejunal motility in an intensity-dependent manner, via a mechanism in which sympathetic nerves and TRPV1 receptors play an important role.


Electroacupuncture; Gastrointestinal disorder; Jejunal motility; Sympathetic nervous system; Transient receptor potential vanilloid-1

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