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尾状核阿片肽可能参与针刺镇痛。

Possible involvement of opioid peptides of caudate nucleus in acupuncture analgesia.

作者信息

Lianfang He, Ruiliang Lu, Shouyuan Zhuang, Xuegui Zhang, Xiaoping Pan

机构信息

Laboratory of Neurophysiology and Neurochemistry, Research Department of Acupuncture, Shanghai First Medical College, ShanghaiPeople's Rep. of China.

出版信息

Pain. 1985 Sep;23(1):83-93. doi: 10.1016/0304-3959(85)90233-7.

Abstract

Rabbits chronically implanted with permanent cannulae were used in brain perfusion and microinjection experiments. Potassium iontophoresis applied to the rabbits' ear skin served as a noxious stimulus and the electric current used to elicit the defense response was taken as the pain threshold. The brain perfusate was analysed by radioreceptor assay and the level of endogenous opioid peptides (EOP) was expressed as competition rate. Electroacupuncture (EA) elicited an increase in pain threshold and a rise in EOP level in the perfusate from the anterior part of the head of the caudate nucleus (n = 10, P less than 0.002) but not from the posterior part. The pain threshold raising effect of EA could readily be reversed by microinjection of naloxone into the anterodorsal part of the head of the caudate (n = 12, P less than 0.01). With the techniques of multimicropipettes and microiontophoresis, caudate neuronal activity was recorded and examined in acute animals anesthetized with chloralose and urethane. It was found that microiontophoresed etorphine produced a strong, naloxone reversible inhibition of the spontaneous activity of the caudate neurons (61/162). Most etorphine sensitive neurons were identified in the dorsal part of the head of the caudate (P less than 0.01). EA produced inhibition of some etorphine sensitive neurons (16/35) and the inhibition could also be reversed by microiontophoresis of naloxone (4/8). The results indicate the participation of intracaudate opioid peptides in acupuncture analgesia.

摘要

在脑灌注和微量注射实验中使用长期植入永久性套管的兔子。将钾离子透入法应用于兔子的耳部皮肤作为有害刺激,用于引发防御反应的电流被视为疼痛阈值。通过放射受体分析法分析脑灌注液,内源性阿片肽(EOP)水平以竞争率表示。电针(EA)使尾状核头部前部灌注液中的疼痛阈值升高且EOP水平上升(n = 10,P < 0.002),但后部未出现这种情况。将纳洛酮微量注射到尾状核头部前背部可轻易逆转电针的疼痛阈值升高效应(n = 12,P < 0.01)。采用多微吸管和微离子透入技术,在使用水合氯醛和氨基甲酸乙酯麻醉的急性动物中记录并检测尾状核神经元活动。发现微离子透入埃托啡对尾状核神经元的自发活动产生强烈的、纳洛酮可逆转的抑制作用(61/162)。大多数对埃托啡敏感的神经元在尾状核头部的背侧被识别出来(P < 0.01)。电针抑制了一些对埃托啡敏感的神经元(16/35),且这种抑制作用也可通过纳洛酮微离子透入逆转(4/8)。结果表明尾状核内阿片肽参与针刺镇痛。

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