Medical Research

Spinal Serotonin and Electroacupuncture: University of Maryland Group

Kristen Sparrow • February 11, 2012

University of Maryland with another elegant study exploring the precise spinal neuro-receptors involved in electroacupuncture. They employ the model that they have used repeatedly, iwhich is to inject Freund’s adjuvant into the joint space of cats hind paws. This is an irritant which mimics arthritis. They then use hind paw withdrawal latency to measure the effects of acupuncture versus control.
But don’t we all know that acupuncture is just placebo??
(Information on my practice here.)

Involvement of spinal serotonin receptors in electroacupuncture anti-hyperalgesia in an inflammatory pain rat model.
Zhang Y, Li A, Xin J, Lao L, Ren K, Berman BM, Tan M, Zhang RX.
Neurochem Res. 2011 Oct;36(10):1785-92.
Center for Integrative Medicine, School of Medicine, University of Maryland, 685 W Baltimore street, MSTF Rm 8-22, Baltimore, MD 21201, USA.

We previously showed that electroacupuncture (EA) activates medulla-spinal serotonin-containing neurons. The present study investigated the effects of intrathecal 5,7-dihydroxytryptamine creatinine sulfate, a selective neurotoxin for serotonergic terminals, the 5-hydroxytryptamine 1A receptor (5-HT1AR) antagonist NAN-190 hydrobromide and the 5-HT2C receptor (5-HT2CR) antagonist SB-242,084 on EA anti-hyperalgesia. EA was given twice at acupoint GB30 after complete Freund’s adjuvant (CFA) injection into hind paw. CFA-induced hyperalgesia was measured by assessing hind paw withdrawal latency (PWL) to a noxious thermal stimulus 30 min post-EA. Serotonin depletion and the 5-HT1AR antagonist blocked EA anti-hyperalgesia; the 5-HT2CR antagonist did not. Immunohistochemical staining showed that spinal 5-HT1AR was expressed and that 5-HT2CR was absent in naive and CFA-injected animals 2.5 h post-CFA. These results show a correlation between EA anti-hyperalgesia and receptor expression. Collectively, the data show that EA activates supraspinal serotonin neurons to release 5-HT, which acts on spinal 5-HT1AR to inhibit hyperalgesia.