电刺激中脑中央灰质对中缝大核神经元放电的影响及纳洛酮效应

<正> 延脑中缝大核(NRM)是中枢下行抑制系统的重要核团之一,电针能够激活NRM而镇痛,损毁NRM或其到达脊髓的主要下行通路背外侧索,可减弱或消除电针的镇痛作用。我们以往的工作观察到,局部导入吗啡拮抗剂纳洛酮可阻断电针对NRM神经元的激活作用,提示内源性吗啡样物质(MLS)参与调制。那么作用于NRM的MLS从哪里来?近年来研究表明,中脑导水管周围灰质(PAG)和第三脑室周

THE EFFECT OF PAG STIMULATION ON NRM NEURONAL ACTIVITY AND ITS BLOCKADE BY IONTOPHORETIC NALOXONE

In our previous work, the activation of nucleus raphe magnus (NRN) by acupuncture could be blocked by iontophoretic naloxone, Suggesting that the endogenous opiate-like substance (OLS) may be involved in it. It is well known that the Periaqueductal qray matter (PAG) which is rich in enkephalin-containing neurons and opiate receptors, could be activated by acupuncture and the content of the OLS in PAG perfusate could be elevated by acupuncture, so it is reasonable to suppose that the activation of NRN may be at least in part due to the OLS released from PAG and other stru- ctures. In the present sludy the effects of dorsal and ventral PAG stimuletion on NRN neuronal activities were observed, throuqh a pais of concentric electrodes implan ted into PAG to further investigate the role of PAG in the activation of NRN by acupuncture. The experiments were carried out on adult male rats. Among 23 NRN neurons, the firinq rate of 12 neurons was increased following the dorsal PAG stimulation (0.5ms, 400μA), only that of 4 neurrons was decreased and the remaining 7 neurons showed no change.The mean firing rate was increased up to 140% of the pre-stimulation value and it was of statistically significance (P<0.05). When naloxone was iontophoretically ejected for two minutes on 9 NRN neurons which were excited by dorsal PAG stimulation, the excitatory eff- ect of 6 neurons was prevented and that of one neuron was reduced, and the other two neurons had no change. It indicates that the activaton of NRN by dorsal PAG stimulation may be mediated by OLS released from the enkephalin-containing neurons eocated in dorsal-PAG, it may be of im- portance in acupuncture analgesia. In contrast, among 22 NRN neurons only 5 neurons were activated by ventral-PAG stimulation, 9 neurons were inhibited and 8 neurons showed no change. The mean firing rate was only reduced to 80% of the pre-sti- mulation control value, it was of no significance. It is supposed that there exist some inhibitory interneurons which were sensitive to opioid peptides and sent their tonic inhibitory influence upon the enkephalin-cntaining neu- rons naturally. When they were excited by electrical stimulation, the ir ton- ic inhibitory effect was enhanced, thus the activatin of NRN neurons was reduced. However, the detailed mechanism of analgesia produced ky ventr- al-PAG stimulattion remains to be further studied.