我国多年来关于针刺镇痛原理的研究表明

针刺镇痛作用是通过神经系统实现的。近年来证明脑内存在有内在的痛控制系统。它可通过延脑中缝大核下行抑制脊髓背角神经元

阻止痛信息的传入而起到镇痛作用。我们和一些研究者报道了刺激NRM可加强针刺的镇痛作用

而毁损NRM可使针刺的镇痛作用减弱。近来我们直接记录NRM神经元放电看到电针可激活NRM神经元的自发放电并抑制其伤害性反应

而且纳洛酮可以翻转此种效应Our Previous work demonstrated that the neurons of nucleus raphe magn- us(NRM) were activated and their nociceptive responses were inhibited by ele- ctroacupuncture(EA) of Zusanli point in rats and this effect could be reversed dy naloxone. The results suggest that the effect of EA on NRM

which consti- tutes a main origin in the descending inhibitory system

is mediated by endorph ine. However

it is known that periaqueductal gray matter(PAG)is dense with- opiat receptors ana rich in endorphine. It is a sensitive area that general an- algesia can be evoked by microinjection of morphine and local electrical stimula- tion. And there exists a close relation between PAG and NRM. The aim of the present work is to study the modulation of PAG on neurons of NRM and its role in electro-acupuncture analgesia(EAA). Experiments were performed on male rats anesthetized with urethane(lmg /kg). The spontaneous discharge of NRM unit and its nociceptive response in- duced by train impulses(frequency: 100Hz

train length: 50-100mSec

duration: 0.5 mSec

intensity: 20-30V)stimulation on rats tail were recorded extracellularly with glass microelectrode. 1. The EA of bilateral Zusanli point for 5 minutes could activate the majority of the neurons of NRM

increasing their unit discharges and inhi- biting their nociceptive responses. The changes

lasting about 20 minutes after EA

as compared with the basal values obtained before EA

were statistically significant(P<0.05-0.001). 2. When the noxious stimulus was excessively strong or repeatedly used

the stimulus itself could activate the unit discharge and inhibite the nocicep- tive response of NRM like EA. 3. After bilateral lesion of PAG with electrolysis (300μA

0.5-1 minute) the level of unit discharge of NRM was increased. The activation on unit di- scharge and the inhibition on nociceptive response induced by EA were mar- kedly diminished or completely disappeared

and in some cases the nocicep- tive response even appeared enhanced. In the control group and in animals with bilateral lesion of PAG

the differance of EA effect estimated by unit discharge at 0 minute and nociceptive response within the initial 20 minutes was statistically significant(P<0.05-0.001). 4. In the rat with bilateral lesion of PAG

the inhibition of fentanyl(50μg /kg) on nociceptive response of NRM unit was also markedly diminished or disappeared. 5. When PAG was stimulated with continuous impulse for 10 sec (frequen- cy: 40Hz

wave width: 0.1mSec

current: 300-500μA)

the discharge of NRM unit was increased and its nociceptive response decreased. The action of stimulat- ing PAG was stronger than EA. The effects of stimulating PAG exerted upon neuron of NRM could be reversed by naloxone(1mg/kg

I.p.). The activation of the neurons of NRM is supposed to be mediated by endorphine. The above results suggest that the effects of EA

fentanyl and stimulat- ing PAG have some common characteristics. They were closely related to PAG and NRM in the cycle of endorphine-mediated analgesic system. The noxious stimulation can also activate the mechanism of analgesia

leading to negative feedback on input of pain. The above results also indicate that PAG possesses the property of exert- ing both excitatory and inhibitory actions upon the neurons of NRM. It is conjectured that EA may result in the release of endorphine by the enkeph- alinergic neurons or other neurohumeral mechanism

directly or indirectly ac- tivate the excitatory function of PAG and suppress its inhibition on NRM. It

in turn

activates the ascending inhibitory system of NRM and other path- ways to restrict the entrance of pain impulse

and thus finally produces electro- aupuncture analgesia.