在尾核痛反应神经元和整体甩尾反射水平上研究辛卡利特对抗电针的镇痛作用

Study on the Antagonism of Sincalide to the Analgesic Effect of Electroacupuncture from Reactions of Pain-related Neurons of Caudate Nucleus and Behavior in Rats

目的:研究辛卡利特(CCK-8)对抗电针(EA)对大鼠尾核(Cd)中痛反应神经元放电和甩尾潜伏期(TFL)痛阈的影响。方法:采用了同步记录大鼠Cd中痛兴奋神经元(PEN)或痛抑制神经元(PIN)电变化与辐射热照射大鼠尾所引起TFL的方法。实验分3组:①对照组:不给大鼠任何处理。②EA组:用G-6805型治疗仪,电压6 V,频率15 Hz,连续电脉冲,刺激双侧“足三里”15 min。③EA+CCK-8组:在EA双侧“足三里”15 min后,借助自动微量推进器立即向大鼠侧脑室注入CCK-8(10 ng/10μL),2 min注射完毕。结果:辐射热照射大鼠尾可使PEN诱发放电增加或PIN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;EA双侧“足三里”15 min可抑制PEN的电活动或加强PIN的电活动,同时使TFL延长,即呈现出EA的镇痛效应;侧脑室注射CCK-8能同时对抗EA所引起PEN或PIN和TFL的镇痛作用。结论:CCK-8的抗EA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。提示降低脑内CCK-8的含量能提高临床针刺的镇痛疗效,以及PEN和PIN的电活动作为疼痛和镇痛指标是确实可行的。

Objective： To observe the effect of intracerebroventrioular （icv） injection of Sincalide （CCK-8） on the electrcacupuncture （EA） analgesia by using discharges of neurons of Caudate nucleus （Cd） and radiant heat irradiation induced tail- flick reflex as the indexes, Methods： Eighty-six Wistar rats anesthetized by 20% urethane （1.0 g/kg） were randomized into control, EA and EA＋ CCK-8 groups, Extracellular discharges of pain-excited neurons （PEN） and pain-inhibitory neurons （PIN） in Cd were recorded by using glass micropipettes （0.5- 1.0μm in diameter, 10-30mΩ in resistance）. Radiant heat irradiation intail-flick latency （TFL） was used as the pain threshold index. EA （6 V, 15 Hz and continuous electric pulses） was applied to bilateral ＂Zusanll＂ （ST 36） for 15 min. Fifteen minutes after EA stimulation, CCK-8 （ 10 ng/10μL） was injected slowly into the lateral cerebral ventricle （A： -0.2 mrn; R：1. 5 mm; H：3.0 mm） in a duration of 2 min. Results： 1） A total of 105 neurons including 63 PEN and 42 PIN were recorded in Cd. The radiant heat induced TFL simultaneously caused an increase in the discharge of PEN or a reduction in that of PIN, showing a painful effect of radiant heat on both the rat＇s behavior and central neuronal activity. 2） EA at bilateral ＂Zusanli＂ （ST 36） resulted in an inhibition of the electrical activity of PEN as well as a potentiation of the electrical activity of PIN and a prolongation of TFL, exhibiting an analgesic effect of EA, 3） The analgesic effect of EA on PEN or PINand TFL were simultaneously antagonized by icv injection of CCK-8 （10 ng/10μL）. Conclusion： The antagonism of CCK-8 to analgesic effect of EA shows the coordinative and consistent actions on the levels of discharges of central pain-related neurons and the whole behavior reflex. It suggests that reducing concentration of CCK-8 in the brain can potentiate the analgesic effect of clinical acupuncture, and the electrical activities of PEN and PIN being as the indexes of pain and analgesia are indeed feasible.