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以截肢造成的创伤痛作为动物模型，用玻璃微电极细胞外记录大鼠下丘脑背内侧核（ＤＭＨ）神经元的放电，观察到：（１）创伤痛大鼠ＤＭＨ自发放电的单位总数比正常大鼠明显减少，但痛敏单位数无明显变化；（２）电针“足三里”和“三阴交”后，ＤＭＨ痛兴奋单位的自发放电和痛诱发放电的频率明显减少，且痛诱发放电的时程明显缩短；ＤＭＨ痛抑制单位的自发放电频率增加，并解除伤害性刺激引起的抑制效应。结果提示：外周伤害性刺激的持续性传入能一定程度地抑制ＤＭＨ的电活动，而ＤＭＨ电活动的受抑可能是慢性痛状态下痛觉过敏的中枢机理之一；电针穴位的传入信息与伤害性刺激的传入信息在中枢的不同水平上相互作用，使疼痛信息受到抑制，从而使ＤＭＨ的功能活动得以恢复，这可能是慢性痛状态下电针镇痛的原理之一。
Taking the traumatic pain caused by amputation as an animal model, the discharge of the hypothalamic dorsal medial nucleus (DMH) neurons was recorded extracellularly by glass microelectrode. The results showed that: (1) The total number of spontaneous discharges of DMH in traumatic pain rats was higher than normal (2) After electro-acupuncture at “Zusanli” and “Sanyinjiao”, the frequency of spontaneous discharge and pain-induced discharge of DMH pain excitement unit decreased obviously, and the pain-induced discharge Time course was significantly shortened; spontaneous discharge frequency of DMH pain inhibition units increased, and to lift the inhibitory effect of nociceptive stimuli. The results suggest that the persistent afferent of peripheral noxious stimulation can inhibit the electrical activity of DMH to a certain degree, while the inhibition of DMH electrical activity may be one of the central mechanisms of hyperalgesia in chronic pain state. Interaction with nociceptive stimuli at different levels of the central nervous system suppresses pain information and thereby regains functional activity in DMH, which may be one of the mechanisms of EA analgesia in chronic pain states.