我们以往的工作证明电解损毁双侧大鼠伏核后可以减弱电针激活中缝大核(NRM)神经元自发放电和抑制伤害性反应的效应。但伏核是通过什么递质和途径参与这种作用的?这一问题值得进一步探讨。方法实验用雄性大白鼠体重250～350克。麻醉、外科手术、NRM单位放电记录和脑刺激等技术方法与以往工作相同。微量注射是用微量注射器

取5微克/1微升的纳洛酮溶液0.3～0.5微升

在微电极推Our previous work demonstrated that the activation of electroacupunc- ture (EA) of "Zusanli" point on neurons of N. raphe mgnus (NRN) could be reduced by lesion made on bilateral N. accumbens (NAC). But by what mediator and what pathway

the N. accumbens participated in the effects of EA on NRM neurons? The Prupose of the present work was to analyze this problem. Experiments were Performed on male rats (250-350).The unit discharges of NRM was recorded extracellularly with glass microelectrode

and the technique of microinjection was employed.The results obtained were as follows: 1. After microinjection of naloxone into bilateral N. accumbens (2.5μg/ 0.5μl to each side)

The effects of EA of "Zusanli" point on NRM neurons (n=12) could clearly be blocked. Comparing with the control before EA

no clear changes were induced but comparing with the control group in wh- ch NRM neurons were injected with normal saline (n=9)

the difference brtween the effects of EA on them was striking. Spontaneous discharge at O min (P<0.01) and nociceptive responses at 0

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10

and 20 min were statistically significant (P<0.05～0.01). It is probably that endorphin in N. accumbens may be a possible mediator Participating in the effect of EA on NRM neurons. 2. The stimulation of N. accumbens could activate the spontaneous dis- charge of the excitatory neurons of NRM (n=13) and inhibit their nocic- eptive responses. Comparing with the control before stmulation

the former at O min (P<0.01) and the latter at 0

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20 and 30 min (P<0.05-0.01) after stimulation were statistically significant. It suggested that the N. ac- cumbens exerted probably control of NRM. 3. Aftermicroinjection of naloxone (1.5-2.5μg/0.3-0.5μl (into periaqu- eduetal grar (PAG)

the effects of stimulation of NAC upon the excitatory neurons of NRM (n=13) were clearly blocked in a majority. Comparting with the control before stimulation

the spontaneous discharges and nocice- ptive responses showed no definite changes

but control group microinjec- ted with normal saline into PAG (n=11)

the spontaneous discharges at 20 min (P<0.05) and the nociceptive responses at 0

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10 and 20 min (P< 0.05-0.01) were statististically significant. The above results showed that N. accumbens probably participated in the effect of EA on NRM neurons dirrectly or indirectly via endorphin in NAC and PAG

which in turn

could activate the NRM

a descending pain inhibitory system

thus achieving analgesia.