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UBC Theses and Dissertations

Supraspinal involvement in acupuncture analgesia Yee, K.C.


Electroacupuncture (EA) on Zusanli (st. 36) and Shangjuxu (st. 38) (10 Hz, 1.0 ms) was found to produce a long-lasting inhibition of wide dynamic range neurones in the dorsal horn of the spinal cord and to prolong the latency of the tail-flick reflex in the lightly anaesthetized rat. This inhibition was effectively produced at a stimulation intensity which excited only A13 fibres. The effects of EA were eliminated by cold-blocking the spinal cord rostral to the recording site suggesting a supraspinal involvement in the EA-induced inhibition of spinal cord nociceptive transmission. EA also facilitated the discharge of non-clock-like dorsal raphe neurones (NCL). Bilateral lesions of the ventrolateral tract (VLT), but not the dorsolateral funiculi (DLF), blocked this effect suggesting that the ascending arm of the loop is via the VLT. The descending arm is located in the DLF since bilateral lesions of the DLF blocked the effects of EA in the spinal cord. Evidence in the literature suggests that the dorsal raphe nucleus (DRN) may be involved in the above supraspinal loop as well as in an ascending inhibitory pathway to the nucleus parafascicularis (NPF). Examination of the DRN revealed three types of neurones: clock-like (CL), NCL and non-clock-like non-responding neurones (NCLN). The NCL neurones were excited by noxious and non-noxious natural peripheral stimuli as well as EA. The other neurones were non-responsive to these stimuli. NCL neurones of the DRN were also antidromically activated by 11 NPF stimulation indicating that the projection from the DRN to the NPF is direct. Stimulation of the DRN produced an inhibition of NPF neurones with sudden onset and offset and a duration correlated with the length of stimulation. EA also produced long-lasting inhibition of these cells. The inhibitory pathway from the DRN to the NPF, which is activated by EA and presumably mediated by NCL neurones, would appear to be serotonergic. The evidence for this is that the inhibition evoked by DRN stimulation or EA is enhanced by alaproclate, a 5-FIT uptake blocker, and blocked by 5,7-DHT, a 5-HT neurotoxic agent, or cyproheptadine, a serotonin antagonist.

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