八肽胆囊收缩素对抗电针对大鼠尾核痛反应神经元电活动和甩尾痛阈的同时影响

许多资料表明 ,八肽胆囊收缩素 (ＣＣＫ 8)能对抗阿片物质的镇痛作用。实验用雄性Ｗｉｓｔａｒ大鼠 30只 ,用 2 0 %氨基甲酸乙酯 (1 .0 ｇ/ｋｇ体重 )麻醉下实施常规手术。以辐射热照射大鼠尾部作为伤害性刺激 ,用玻璃微电极引导尾核中痛反应神经元放电。本实验以大鼠尾核中痛兴奋神经元(ＰＥＮ)和痛抑制神经元 (ＰＩＮ)的电变化及甩尾反射潜伏期 (ＴＦＬ)三者为指标 ,研究了脑室注射1 5ｎｇＣＣＫ 8对抗电针对尾核痛反应神经元放电和甩尾痛阈的同时作用。结果 :①辐射热照尾可使大鼠尾核中ＰＥＮ痛诱发放电频率增加、诱发放电潜伏期缩短或…

Involvement of Cholecystokinin Octapeptide in Electroacupuncture Inhibiting Electrical Activities of Pain-related Neurons in Caudate Nucleus and Raising Pain Threshold of Tail Flick in Rats

Objective: To study the influence of intra cerebroventricular injection of cholecystokinin octapeptide (CCK 8) on the effect of electroacupuncture (EA) i n antagonizing the electrical activity of pain related neurons in caudate nucle us (Cd) and raising pain threshold.Methods: 30 male Wistar rats were used. Operations were performed under general anesthesia with 20% urethane (1.0 g/kg of body weight). The radiant heat irradiation (nociceptive stimulus) induce d rat tail flick reaction was used as the pain index. Extracellular discharges o f pain related neurons pain excitatory neurons (PEN) and pain inhibitory ne urons (PIN) in Cd and tail flick latency (TFL) before and after cerebroventri cular microinjection of CCK 8 (15 ng) were recorded. Electroacupuncture (EA) wa s applied to bilateral "Zusanli" (ST 36).Results: ① The radiant heat focused on the tail of rats caused increase of the pain evoked discharging frequency and shortening of the evoked discharging latency of PEN or reduction of the pain evoked discharging frequency and prolongation of the inhibitory du ration of the evoked discharges of PIN and generated tail flick reflex simultaneously. ② EA of bilateral "Zusanli" (ST 36) for 15 min resulted in inh ibition of the electric activity of PEN as well as potentiation of the electrica l activity of PIN and a prolongation of tail flick latency (TFL), i.e. exhibitin g the analgesic effect of EA. The effects peaked immediately after EA, the net i ncrease value (NIV) of the pain evoked discharges of 19 PENs was reduced from 1 6.17±2.30 Hz to 5.45±2.96 Hz and TFL was prolonged from 5.03±0.31 sec to 8.89 ±0.58 sec simultaneously, the inhibitory duration of the pain evoked discharge s of 12 PINs was shortened from 5.19±0.24 sec to 2.52±0.33 sec and TFL was pro longed from 4.57±0.23 sec to 8.12±0.29 sec simultaneously. These changes recov ered gradually 10 min after EA. ③ The inhibitory effect of EA on the pain evok ed discharges of PEN and the potentiated effect of EA on the electric activities of PIN, and the prolonged effect of EA on TFL were antagonized by intra cerebr oventricular injection of 15 ng CCK 8, i.e. CCK 8 could antagonize the analges ic effect of EA. About 4 min after injection of CCK 8, the effects were most ap parent. Very soon after EA, the NIV of 13 PENs was reduced from 9.36±2.10 Hz to 2.34±0.46 Hz and TFL was prolonged from 5. 38±0.18 sec to 8.60±0.49 sec simu ltaneously, the inhibitory duration of 10 PINs was shortened from 5.54±0.32 sec to 2.09±0.79 sec and TFL was prolonged from 4.92±0.17 sec to 9.44±0.21 sec s imultaneously. About 4 min after injection of CCK 8, the NIV of PENs was recov ered to 7.44± 1.38 Hz and TFL to 5.53±0.19 sec, the inhibitory duration of PINs was recovered to 6.20± 0.61 sec and TFL to 4.54±0.16 sec. About 14 min after injection of CCK 8, it gradually recovered. Conclusion: T he results demonstrate that the antagonism of CCK 8 on analgesic effect of EA s hows a coordinated and consistent action at the levels of electrical activity of central neurons and the whole behavior reaction.