RELATIONSHIP BETWEEN ELECTROACUPUNCTURE ANALGESIA AND DESCENDING PAIN INHIBITORY MECHANISM OF NUCLEUS RAPHE MAGNUS
RELATIONSHIP BETWEEN ELECTROACUPUNCTURE ANALGESIA AND DESCENDING PAIN INHIBITORY MECHANISM OF NUCLEUS RAPHE MAGNUS
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DOI：
10.1016/0304-3959(86)90124-7
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发表时间：
1986-03-01
期刊：
影响因子：
7.4
通讯作者：
ZHANG, SX
中科院分区：
文献类型：
--
作者：
LIU, X;ZHU, B;ZHANG, SX
中缝-脊髓（R-S）神经元位于中缝大核（NRM）。其轴突的传导速度计算为约15-60米/秒。绝大多数R-S神经元对非伤害性刺激（如梳理头发或轻轻按压皮肤）没有明显反应，但它们对伤害性刺激（针刺或夹住）有反应，其放电率增加或减少。R-S神经元对伤害性刺激的感受野很广，几乎覆盖全身。R-S神经元对伤害性刺激的反应类型为兴奋性（放电频率增加）、抑制性（放电频率减少）和无反应型，意外发现3个可逆性兴奋-抑制型R-S神经元，抑制性R-S神经元的放电频率高于兴奋性R-S神经元。兴奋-抑制可逆神经元对伤害性刺激的反应也与背景放电频率有关。电针对兴奋性R-S神经元的作用主要是增加其放电频率，抑制其伤害性反应。切断DLF后，电针仍能激活R-S神经元，但电针对R-S神经元伤害性反应的后抑制作用明显减弱。提示电针可激活脊髓上的NRM区，通过下行抑制介导痛觉负反馈通路，从而产生镇痛作用。
Raphe-spinal (R-S) neurons were identified in the nucleus raphe magnus (NRM). The conduction velocity of their axons was calculated to be about 15-60 m/sec. The great majority of R-S neurons did not respond clearly to non-noxious stimuli, such as brushing hair or lightly pressing the skin, but they did respond to noxious stimuli (pricking or clamping), with increases or decreases in their firing rates. The receptive fields of the R-S neurons responding to noxious stimuli were very wide covering almost all of the body. The responses of R-S neurons to noxious stimulation were excitatory (increasing firing rates), inhibitory (decreasing) and unresponsive in type, and we unexpectedly found 3 reversibly excitatory-inhibitory type R-S neurons, the firing rate of inhibitory R-S neurons being higher than that of excitatory R-S neurons. The responses of the excitatory-inhibitory reversible neurons to noxious stimulation were also related to the background firing rates. The effects of electroacupuncture (EA) on the excitatory R-S neurons were mainly to increase their firing rates, and to inhibit their nociceptive responses. After the transection of DLF, the R-S neurons could still be activated by EA, but the post-inhibitory effects of EA on their nociceptive responses were obviously reduced. It is suggested that the EA can activate NRM, a supraspinal area mediating a negative feedback circuit modulating pain, thus inducing analgesia via descending inhibition.