许多工作证明

作为第二信使的环核苷酸可能参与了痛觉的调节机制。我们曾经观察了电针镇痛时大鼠全脑及各脑区环-磷酸腺苷(cAMP)环-磷酸鸟苷(cGMP)含量的变化。发现电针镇痛时端脑cAMP含量下降

而脑干部位cGMP明显升高

这些变化可被阿片受体阻断剂纳洛酮所翻转。反复电针时

电针镇痛作用会逐渐下降发生Groups of rats were decapitated after 30 min electroacupuncture (EA) on bilateral Zusanli-Sanyinjiao points. The analgesic effect of EA was expressed by the percent change of the tail flick latency

and the brain cAMP and cGMP content measured by protein binding and radio-immunoassay respectively. EA stimulation for 30 min (one session) caused a significant increase in tail flick latency. In the meantime there was a significant decrease of cAMP content (-23%

p<0.05) in telencephalon

as well as a decrease of cGMP in diencephalon(-25%

p<0.05) and an increase of cGMP(+43%

p<0.05)in lower brain stem. Repeated EA stimulation for 6 sessions

with 30 min 'intervening between successive sessions

resulted in a gradual decrease and final disappearance of its analgesic effect

which was termed "EA tolerance". Cyclic nucleotides measurement revealed that in EA tolerant rat the cAMP content of the telencephalon remained in a low level as was in EA analgesic rats. However

the characteristic changes in cGMP content found in EA analgesic rats were no longer existing in EA tolerant rat. The most impressive increase in cGMP content in the lower brain stem was completely abolished. That the inability to raise cGMP content in lower brain stem may be partially responsible for the development of EA tolerance was supported by the fact that the effect of EA analgesia could be partially restored by intracerebroventricular injection of 100μg of cGMP

a dose which by itself was not analgesic. The results indicate that an insufficient supply of cGMP during repeated or prolonged EA stimulation may constitute one of the mechanisms for the diminution of the analgesic effect during EA tolerance.