比较电针“合谷”对中缝大核神经元由首尾不同部位伤害性刺激所引起痛反应的抑制效应

<正> 近年来研究证明脑内存在有以脑室周围灰质和导水管周围灰质为中心的镇痛系统。它可以通过延髓的下行抑制通路,阻遏脊髓背角痛信息的输入而起到镇痛作用。我们以往的工作多次证明电针“足三里”确实可以激活延脑中缝大核(NRM)这     

穴位相对特异性与经络或神经节段关系的实验研究

本工作选用足少阳胆经的“上关”和“阳陵泉”及与之对应的足阳明胃经的“下关”和“足三里”,但“上关”和“下关”位于头部的颧弓上下,同为三叉神经支配。而“阳陵泉”和“足三里”位于腓骨小头前下方,同受腓总神经支配。分别观察电针这四个穴位对中缝大核（NRM）神经元及其由牙髓或尾尖饬害性刺激所引起的反应的效应,分析穴位相对特异性与经线或神经支配节段性的关系。观察到电针“上关”和“下关”均可激活NRM神经元,并抑制其两种刺激所引起的伤害性反应。但对牙髓伤害性反应的抑制作用更强（约－60％,5～10分,P＜0．05～0．001）,而对尾尖伤害性反应无明显的抑制作用或仅为－30％。电针“阳陵泉”或“足三里”也可激活NRM神经元并抑制两种伤害性反应,但对尾尖伤害性刺激反应的抑制作用比对牙髓的强而持久,前者为－60％～－40％,30分钟（P＜0．05～0．001）,后者为－40％,5～10分钟（P＜0．05～0．001）。上述事实表明,头部穴位电针对牙痛,后腿穴位电针对尾部痛的镇痛作用更好。指出穴位相对特异性似不依经线区分,而与神经支配的节段性关系密切。     

大脑皮层体感Ⅱ区对中缝大核下行痛抑制活动的调控及其与电针镇痛的关系

用玻璃微电极细胞外记录大鼠(NRM)神经元单位放电及其对尾尖伤害性刺激的反应,研究表明刺激 SmⅡ可增加 NRM 神经元的自发放电,抑制其伤害性反应;与电针对 NRM 的效应相似,发现两者具有相关性。提示:SmⅡ对 NRM 镇痛机制可以发挥下行性调控,电针对 NRM 的影响可能部分是经激活 SmⅡ,再转而作用于 NRM 的。     

损毁大鼠大脑皮层体感Ⅱ区导致电针对中缝大核痛调制的效应减弱

以往曾证明刺激皮层体感Ⅱ区（SmⅡ）可以激活具有下行痛调制机能的中缝大核（NRM）,神经元自发放电增多,伤害性反应受到抑制,而且刺激SmⅡ的这种效应与电针“足三里”所引起的效应成正相关关系（P＜0．001）,表明两者有某种共同中枢机制。本文的工作进一步证明电解损毁SmⅡ区,可削弱电针“足三里”激活NRM神经元和抑制伤害性反应的作用。表明SmⅡ区参与电针镇痛,它的结构和机能的完整是电针镇痛所必须的,但不是唯一的结构。因SmⅡ损毁后电针的镇痛效应并未完全消失,可能还可通过其它中枢结构,参与内源性镇痛系统的作用,而产生一定的镇痛作用。     

感觉运动皮层的锥体束通路对NRM电针镇痛效应的影响

感觉运动皮层可通过锥体束及锥体外系对躯体运动进行控制。本实验证明大鼠感觉运动皮层也可通过锥体束对痛觉进行调制。锥体束切断后可明显增强电针“足三里”的镇痛作用。表明锥体束完整的情况下对电针的镇痛效应有拮抗作用。这可能是患者情绪急躁全身肌肉紧张时,针刺疗效不佳的机制之一。     

The role of negative feedback modulating pain of nucleus raphe magnus in electroacupuncture analgesia

In recent years I am interested in the role of nucleus raphe magnus (NRM) in acupuncture analgesia, NRM is the one of important descending inhibitory systems included in the intrinsic analgesic systems in brain, and we gave more systematic study on the question. The primary results are as follows: 1. Experiments were performed on male rats, unit discharges of NRM were recorded extracellularly with glass electrode. The neurons respond to noxious stimulation were chosen to observe analgesia of EA. The spontaneous firing rates of NRM neurons were about 0.5-20 Hz, a few of them over 20Hz or have no any discharges. NRM neurons have not often responses to nonnoxious stimulation (to brush hair) or only have a light responses and adaptation appeared fast. But responses of them to noxious stimulation (to clamp or to prick skin) or electro-stimulation (over 6V) were obviously displayed with excitatory (increasing firing rates) or inhibitory (decreasing) types. The spontaneous firing rates of excitatory NRM neurons were lower than that of inhibitory neurons. In addition, a few excitatory-inhibitory reversible type NRM neurons were found unexpected, and the reversal of response were related to background firing rates. During low firing rates, the response was an excitatory one, and during high firing rates, it became an inhibitory one. 2. EA of 'Zusanli' could activate NRM neurons, increasing spontaneous firing rates, and inhibit their nociceptive responses. The effect induced by EA could be reversed by naloxone (I.P.). 3. Raphe-spinal neurons in NRM were identified by antidromic activation and collision technology, their axons project to dorsal horn of spinal cord via dorsal lateral fasciculus (DLF), that seem to be centrifugal units.(ABSTRACT TRUNCATED AT 250 WORDS)     

导水管周围灰质(PAG)对中缝大核(NRM)神经元活动的影响及其在电针足三里镇痛中的作用

<正> 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     

刺激大鼠前额叶对中缝大核神经元放电的影响

<正> 近年来,大脑皮层参与痛觉调制逐渐受到人们的重视。Hardy发现刺激大鼠前额叶(prefrontal cortex,PFC)具有行为镇痛机能,并且观察到刺激PFC可以改变中脑某些神经元的电活动,这些神经     

伏核参与电针对中缝大核神经元效应的途径和机制的分析

<正> 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