摘要
目的:观察八肽胆囊收缩素对抗电针对大鼠束旁核中痛反应神经元放电和甩尾潜伏期痛阈的同时影响及其作用机制。方法:实验于2004-06/2005-04在哈尔滨医科大学神经痛觉电生理研究室完成。选择雄性的Wistar大鼠128只,随机分4组:对照组32只,不给大鼠任何处理。电针组32只,用G-6805型治疗仪给电压6V,频率15Hz,连续的电脉冲刺激双侧“足三里”15min。电针+八肽胆囊收缩素组32只,在电针双侧“足三里”15min后,借助自动微量推进器立即向脑室注入八肽胆囊收缩素(1.5kg/L),2min注射完毕。电针+八肽胆囊收缩素+L-364,718组32只,在注射八肽胆囊收缩素后2min,右侧束旁核内注入八肽胆囊收缩素-A受体拮抗剂L-364,718(100kg/L),2min注射完毕,其他操作同电针+八肽胆囊收缩素组。以辐射热照大鼠尾部背侧下1/3处作为伤害性刺激,引导痛反应神经元的放电。以痛兴奋神经元、痛抑制神经元和甩尾潜伏期的变化作为痛阈的观察指标。当辐射热照大鼠尾开始或甩尾发生时,用SEN-3301电刺激器的电脉冲记号作为照尾和甩尾的标记,与痛兴奋神经元或痛抑制神经元的放电同时显示在VC-9示波器上,从而观察大鼠束旁核中痛反应神经元放电和甩尾潜伏期的同时变化。用GF-777型双道录音机记录这些变化,并输入DAB-1100直方图仪绘制直方图,最后用Z3-304函数记录仪打印。结果:纳入动物128只,均进入结果分析。①辐射热照大鼠尾可使痛兴奋神经元诱发放电增加或痛抑制神经元诱发放电减少的同时发生甩尾反射,表现出辐射热致疼痛效应。②电针双侧“足三里”15min,可抑制痛兴奋神经元的电活动或加强痛抑制神经元的电活动,同时使甩尾潜伏期延长。16个痛兴奋神经元平均净增值从电针前的(12.14±1.31)Hz减少到(3.38±1.92)Hz、同时甩尾潜伏期从(4.79±0.22)s延长到(8.65±0.34)s。9个痛抑制神经元平均抑制时程从电针前(5.34±0.56)s减少至(2.41±0.89)s,甩尾潜伏期从(4.11±0.38)s延长到(8.01±0.59)s,即呈现出电针的镇痛效应。③脑室注射八肽胆囊收缩素能同时对抗电针所引起痛兴奋神经元或痛抑制神经元和甩尾潜伏期的镇痛作用。在电针后立即,15个痛兴奋神经元的平均净增值从电针前100%减少到(17.73±3.05)%,抑制率为(82.27±5.47)%;甩尾潜伏期延长率为(72.83±3.38)%。脑室注射八肽胆囊收缩素后立即,平均净增值的抑制率下降到(15.86±1.82)%;甩尾潜伏期的延长率减少到(13.93±2.12)%。而11个痛抑制神经元平均抑制时程从电针后立即的缩短率为(64.99±8.23)%减少到(11.41±1.58)%;甩尾潜伏期延长率为(60.84±6.28)%下降到(8.63±0.92)%。④束旁核内注入胆囊收缩素-A受体拮抗剂L-364,718能翻转八肽胆囊收缩素对抗电针的镇痛作用。结论:八肽胆囊收缩素的抗电针镇痛作用,在中枢痛反应神经元电活动和整体行为反射水平上是协调一致的,推测该作用是通过胆囊收缩素-A受体而实现的。揭示降低脑内八肽胆囊收缩素的含量或阻断胆囊收缩素-A受体的作用均能提高临床针刺的镇痛疗效以及痛兴奋神经元和痛抑制神经元的电活动作为疼痛和镇痛指标是确实可行的。
AIM： To observe the simultaneous antagonism of cholecystokinin octapeptide to the effects of electroacupuncture on the discharges of painrelated neurons in nucleus parafascicularis and the painful threshold measured by tail-flick latency in rats, and its mechanism.
METHODS： The experiment was conducted in the Institute of Electrophysiological for Neuralgia, Harbin Medical University from June 2004 to April 2005. 128 male Wistar rats were randomly divided into 4 groups： Control group （n=32）： Rats received no disposal. Electroacupuncture group （n=32）： Bilateral ＂zusanli＂ were stimulated continuously with electric pulse （6 V, 15 Hz） generated by G-6805 therapeutic instrument for 15mins. Electroacupuncture ＋ cholecystokinin octapeptide group （n=32）： 15 rains after electroacupuncture at bilateral ＂zusanli＂, cholecystokinin octapeptide （1.5 kg/L） was immediately injected into the lateral ventricle by means of an automatic microadvancemento for 2 mins. Electroacupuncture ＋ cholecystokinin octapeptide ＋ L-364,718 group （n=32）： Two rains after injection of cholecystokinin octapeptide, choleeystokinin octapeptide-A receptor antagonist L-364,718 （100 kg/L） was injected into left parafascicular nucleus for 2 mins, other operations were. same as those in the electroacupuncture ＋ cholecystokinin octapcptide group. The radiant heat focused on one third of the tail in rats was used as a noxious stimulation, so as to lead to the discharges of painrelated neurons. The changes of pain-excited neurons, pain-inhibited neurons, and tail-flick latency were taken as observation indexes of pain threshold. When the radiant heat focused on the tail of rat started or tailflick happened, electric pulse was taken as the marker of radiant heat focused on the tail or tail-flick was sent OUt by SEN-3301 electrostimulator, and showed on the VC-9 oscilloscop accompanied by the discharges of pain-excited neurons or pain-inhibited neurons, so as to observe the simultaneous changes of the discharges of pain-related neurons in the nucleus parafascicularis and tail-flick latency. Changes were recorded with GF-777 tape recorder, then datas were input to DAB-1100 histogram processor to plot the histogram, at last the histogram was printed by Z3-304 function recording instrument.
RESULTS： 128 included rats were involved in the analysis of results.（1）The radiant heat focused on the tail of rats could cause an increase in the evoked discharge of pain-excited neurons or tail-flick reflex at the same time of reducing the evoked discharge of pain-inhibited neurons, showed a painful effect of radiant heat. （2）15 mins of electroacupuncture at bilateral ＂zusanli＂ could inhibit the electrical activity of pain-excited neurons as well as a potentiation of the electrical activity of pain-inhibited neurons, meanwhile, prolong of tail-flick latency. The average net-increased value of 16 pain-excited neumns decreased from （12.14±1.31） Hz before eleetmacupuncture to （3.38± 1.92）Hz, the average tail-flick latency was prolonged from （4.79±0.22） s to （8.65±0.34） s. The average inhibitory duration of 9 pain-inhibited neurons decreased from （5.34±0.56）. s to （2.41±0.89） s, the tail-flick latency was prolonged from （4.11±0.38） s （8.01±0.59） s, i,e. displayed a analgesic effect of electroacupuncture, （3） injection of cholecystokinin octapeptide in the lateral ventricle could simuhaniously antagonize the analgesic eftect of electroaeupuncturc on pain-excited neurons or pain-inhibit neurons and tail-flick latency. immediately after electroacupuncture, the average net-increased value of 15 pain-excited neurons decreased from 100% before electroacupuncture to （17.73±3.05） %, the inhibited rata was （82.27±5,47） %; The prolonged rate of tail-flick latency was （72.83±3.38） %, Immediately after the injection of cholecystokinin octapeptide in the lateral ventricle, the inhibited rate of net-increased value was reduced to （15.86±1.82） %; The prolonged rate of tail-flick latency decreased to （13.93±2.12） %. The shortening rate of the average inhibitory duration of 11 pain-inhibited neurons decreased from （64.99±8.23） % to （11.41±1.58） % immediately after electroacupuncture; The prolonged rate of tail-flick latency was reduced from （60.84±6.28） % to （8.63±0.92） %, （4） The injection of cholecystokinin-Areceptor antagonist U364,718 in parafascicularis nucleus could reverse the antagonism of cholecystokinin octapeptide to the effect of eleetroacupuncture.
CONCLUSION： The antagonism of cholecystokinin octapeptide to analgesic effect of electroacupuncture is coordinative and consistent with the levels of the electrical activities of central pain-related neurons and the whole behaviour reflex, which indicates the antagonistic effect of cholecystokinin octapeptide on electroacupuncture is mainly realized by cholecystokinin-A receptor, It is suggested that reducing content of CCK-8 in brain or blocking effects of cholecystokinin-A receptors can potentiate analgesic effect of clinical electreacupuncture, pain-excited neurons and the electric activity of pain-inhibited neurons, as the index of ache and analgesia, it is feasible.
出处
《中国临床康复》
CAS
CSCD
北大核心
2006年第3期136-139,共4页
Chinese Journal of Clinical Rehabilitation
基金
黑龙江省自然科学基金资助项目(D9603)~~
