乙酰胆碱参与皮层下行调制疼痛的作用

INVOLVEMENT OF ACETYLCHOLINE IN CORTICOFUGAL MODULATION OF PAIN

我们实验室的工作曾报导,刺激猫的皮层SⅡ区、SⅠ区或十字沟前区可抑制丘脑髓板内核群神经元的伤害性反应及针刺镇痛效应。

We have found that after intraperitoneal injecting atropinc the analgesic effect of both stimulating Sm I cortex and acupuncture were decreased. It suggests that acetylcholine (ACh) may be involved in the corticofugal modulation of pain. In order to elucidate this idea the effects of stimulating Sm I cortex on tail flik latency (TFL) after ventrical microinjecting atropine were investigated. The experiments were carried out on Wistar rats. Under the state of anaesthesia a pair of silver ball electrodes were put on the dura for electrical stimulating Sm I and the ipsilateral ventricle was cannulated for microinjecting atropine. Recordings were made 5—6 hours or 24 hours after operation. Immediately after cessation of stimulating SmI and 1'、2'、3.5'、5'、7.5'、10' and 15' later TFL were measured consecutively. The results were as follows: 1. The mean value of TFL was 2,44±0.11 sec (n = 20). It was prolonged (p<0.05) within 0'-5' after stimulation of SmI. Therefore, it indicated that analgesic effects were produced by stimulating SmI cortex. 2. It was found that under the background of microinjecting atropine (10 μg/2μl) TFL remained unchanged after stimulating SmI cortex (n = 10, P> 0.05). There was a significant difference between the two treatments: simple stimulating SmI and atropine plus stimulating SmI at the same animals in TFL (P<0.05) within 0' and 1' after cessation of stimulating SmI. It indicated that the analgesic effects of stimulating SmI cortex were decreased by blocking Mreceptors. 3. Under the background of microinjecting normal saline. The analgesic effects still could be observed after stimulating SmI. The results were just like those obtained in simple stimulating SmI at the same animals (n=10). 4. Comparing atropine group with normal saline group it was shown that there was a statistical difference in TFL at 0' and 1' between the two groups (P<0.05). It suggests that ACh is involved in the corticofugal modulation of pain.