Wang Q, Mao L, Han J
Department of Physiology, Beijing Medical University, People's Republic of China.
Brain Res. 1990 Jun 4;518(1-2):40-6. doi: 10.1016/0006-8993(90)90951-7.
Focal electrical stimulation of the arcuate nucleus of the hypothalamus (ARH) for 5 min (1 session) produced a marked elevation of tail flick latency (TFL) to noxious heat in the pentobarbital-anesthetized rat. Repeated stimulation for a total of 11 sessions at 30 min intervals resulted in a gradual decline in the hypoalgesic action, and this tolerance may last for 7 days. Tolerance to the ARH analgesic stimulation reduced the analgesia produced by low (2 Hz) but not high (100 Hz) frequency electroacupuncture (EA); and tolerance to low frequency EA analgesia attenuated the ARH stimulation-produced analgesia without affecting high frequency EA analgesia. Alternatively, rats tolerant to high-frequency EA analgesia were still sensitive to either the ARH or low-frequency EA stimulation. These results suggest that the ARH stimulation and low-frequency EA administration produced analgesia via a common neural mechanism, supporting our hypothesis put forward previously that the ARH plays an important role in mediating low- but not high-frequency EA analgesia.
对戊巴比妥麻醉的大鼠下丘脑弓状核(ARH)进行5分钟(1次)的局部电刺激,可使对有害热刺激的甩尾潜伏期(TFL)显著延长。以30分钟的间隔重复刺激共11次,可导致镇痛作用逐渐减弱,且这种耐受性可持续7天。对ARH镇痛刺激的耐受性降低了低频率(2Hz)而非高频率(100Hz)电针(EA)产生的镇痛效果;而对低频EA镇痛的耐受性减弱了ARH刺激产生的镇痛效果,且不影响高频EA镇痛。相反,对高频EA镇痛产生耐受性的大鼠对ARH或低频EA刺激仍敏感。这些结果表明,ARH刺激和低频EA给药通过共同的神经机制产生镇痛作用,支持了我们之前提出的假设,即ARH在介导低频而非高频EA镇痛中起重要作用。