Wang Jin-Yan, Zhang Han-Ti, Han Ji-Sheng, Chang Jing-Yu, Woodward Donald J, Luo Fei
Neuroscience Research Institute and Department of Neurobiology, Peking University Health Science Center, 38 Xue Yuan Road, Beijing 100083, PR China.
Brain Res. 2004 Jul 16;1014(1-2):197-208. doi: 10.1016/j.brainres.2004.04.029.
It is well accepted that peripheral electrical stimulation (PES) can produce an analgesic effect in patients with acute and chronic pain. However, the neural basis underlying stimulation-induced analgesia remains unclear. In the present study, we examined the pain-related neural activity modified by peripheral stimulation in rats. The stimulation frequency of pulses applied to needle electrodes in the hindlimb was 2 Hz alternating with 100 Hz, with 0.6 ms pulse width for 2 Hz and 0.2 ms for 100 Hz. The intensity of the stimulation was increased stepwise from 1 to 3 mA with each 1-mA step lasting for 10 min. The nociceptive neural and behavioral responses were examined immediately after the termination of stimulation. Using a multiple-channel recording technique, we simultaneously recorded the activity of many single neurons located in the primary somatosensory and anterior cingulate cortex (ACC), as well as the ventral posterior and medial dorsal thalamus in behaving rats. Our results showed that peripheral electrical stimulation significantly reduced the nociceptive responses in ventroposterior thalamus and somatosensory cortex, indicating an inhibition of nociceptive processing. In contrast, the analgesic stimulation produced a significant increase in mediodorsal thalamus while a less significant decrease in cingulate cortex, reflecting a complicated effect associated with combined antinociceptive activation and nociceptive suppression. These results support the idea that peripheral electrical stimulation can ultimately alter the pain perception by specifically inhibiting the nociceptive transmission in the sensory pathway while mobilizing the antinociceptive action in the affective pathway, thus to produce pain relief.
外周电刺激(PES)可在急慢性疼痛患者中产生镇痛作用,这一点已被广泛接受。然而,刺激诱导镇痛的神经基础仍不清楚。在本研究中,我们检测了外周刺激对大鼠疼痛相关神经活动的影响。施加于后肢针电极的脉冲刺激频率为2Hz与100Hz交替,2Hz时脉冲宽度为0.6ms,100Hz时为0.2ms。刺激强度以1mA的步长从1mA逐步增加至3mA,每步持续10分钟。刺激结束后立即检测伤害性神经和行为反应。使用多通道记录技术,我们同时记录了行为大鼠初级体感皮层、前扣带回皮层(ACC)以及腹后丘脑和背内侧丘脑许多单个神经元的活动。我们的结果表明,外周电刺激显著降低了腹后丘脑和体感皮层的伤害性反应,表明对伤害性处理有抑制作用。相反,镇痛刺激使背内侧丘脑显著增加,而扣带回皮层有较小程度的降低,反映出与抗伤害性激活和伤害性抑制相结合的复杂效应。这些结果支持这样一种观点,即外周电刺激最终可通过特异性抑制感觉通路中的伤害性传递,同时调动情感通路中的抗伤害性作用来改变疼痛感知,从而产生疼痛缓解。