Study on rat hypothalamus arcuate nucleus which plays an important role in the induction of acupuncture analgesia.

为了评估下丘脑弓状核（ARH）在抗感觉系统中的可能作用，我们用雄性Wistar大鼠进行了以下实验。1) ARH病变对疼痛控制和电针镇痛的影响。arh损伤大鼠在30天后的福尔马林测试中疼痛评分明显偏高，表明它们对伤害性刺激过敏。对照组大鼠Ho-Ku处电刺激（3 Hz, 300-600 <微>A）有镇痛作用，而损伤大鼠几乎没有镇痛作用。2) EA对ARH神经元活动的影响。大多数ARH神经元的自发频率在EA刺激下发生显著变化（频率升高或降低）。ARH神经元的活动变化持续约60 min，其时间变化与EA镇痛作用的时间变化一致，说明大部分ARH神经元参与了镇痛作用。3) EA镇痛作用与内源性阿片类药物可能参与的关系。注射纳洛酮（1mg/Kg, ig）可拮抗EA刺激引起的ARH神经元变化和镇痛作用。在EA刺激15 min后立即死亡的动物组，下丘脑内侧基底部< >-内啡肽显著高于对照组。4) ARH刺激对下丘脑外侧区（LHA）神经元活动的影响。ARH刺激（20-45 <micr>A, 1-3 Hz, 30 s）对LHA神经元的自发活动和LHA神经元对有害刺激的反应有抑制作用。因此，ARH调控似乎是中枢疼痛控制系统和EA镇痛诱导的重要组成部分。

To evaluate the possible role of the arcuate nucleus of hypothalamus (ARH) in the antinociceptive system, the following experiments were carried out, using male Wistar rats. 1) The effect of ARH lesion on pain control and electroacupuncture (EA) analgesia. The ARH-lesioned rats showed a significantly high value in pain rating of the formalin test 30 days after, indicating that they were hypersensitive to nociceptive stimuli. An analgesic effect was induced in the control rats by EA stimulation (3 Hz, 300-600 <micr>A) applied at Ho-Ku, but scarcely seen in the lesioned rats. 2) EA effect on the neuronal activity of ARH. The majority of ARH neurons significantly changed their spontaneous frequency rates (the rate increased or decreased) by EA stimulation. The activity change lasted for about 60 min and its time course agreed with that of the analgesic effect of EA. It suggested that the majority of ARH neurons took part in the analgesia. 3) Relationship between tha analgesic effect of the EA and the possible involvement of endogenous opioids. The analgesic effects and the neuronsl change in ARH induced by EA stimulation were both antagonized by injected naloxone (1mg/Kg, i.p.).<bat>-endorphin in the medialbasal hypothalamus was significantly higher in the animal group immediately killed after reciving EA stimulation for 15 min than in the control animal group. 4) The effect of ARH stimulation on the neuronal activity of the lateral hypothalamic area (LHA). ARH stimulation (20-45 <micr>A, 1-3 Hz, 30 s) induced the suppressive effect on the spontaneous activity of the neurons in the LHA and on the response of the LHA neurons to noxious stimuli. ARH resion thus appears to be an important part in the central pain control system and in the induction of EA analgesia.