我们在佐剂诱发的急性关节炎大鼠上研究的结果已经表明

电针穴位和电刺激皮层体感运动Ⅰ区(SmⅠ区)均可明显抑制关节炎鼠丘脑束旁核(Pf)神经元的伤害性反应

用利多卡因局部阻滞SmⅠ区时

电针对Pf神经元伤害性反应的抑制作用削弱

说明皮层SmⅠ区对Pf神经元的伤害性反应Using the adjuvant-induced acute arthritic rat as a pain model

we have previously shown that the Sm I area is implicated in the inhibitory effect of acupuncture on lhe afferent nociceptive information of parafacicular nuclei (Pf). The prupose of this study was to determine whether acetycholine (ACh) participates in this modulatory process. Experiments were conducted with adjuvant-induced acute arthritic rats and cxtracellular recordings from pf were obtained through microelectrodes stereotaxically. The results showed that: (1) After intraperitoneal-injecting atropine (Smg/kg)

the effect of stimulating SmI on nociceptive responses of Pf neurons was decreased

while it was not decreased if saline was administered. Compared in the same neurons

the difference of nociceptive responses at 0′to 15′after cessation of stimulating SmI was staistically sigificant. This finding indicated that ACh was inmolved in descending modulation of SmI.(2) The effect of acupuncture was decreased after intraperitoneal-injecting atropine (Smg/kg)

while it was not decreased if saline was administered.The difference of nociceptive response was statiseically significant at 0′to 10′ and 20′ to 40′ after cessation of EA in comparison between the background of atropine and saline. It indicated that ACh was involved in acupuncture analgesia. These results suggest that ACh may be participated in acupuncture analgesia as a neurotransmitter of the corticofugal modulation of pain.