Wu G J, Chen Z Q
Institute of Acupuncture, China Academy of TCM, Beijing 100700.
Sheng Li Xue Bao. 1999 Feb;51(1):49-54.
The present experiments aimed to investigate whether the caudate nucleus (Cd) was involved in cortical sensorimotor area I (Sm I) generating descending modulation of the parafascicular nucleus (Pf) in acupuncture analgesia (AA), and what type of opiate receptors in Cd were involved. It was found that nociceptive responses of Pf neurons could be inhibited by electroacupuncture (EA) and excitation of Sm I before lesion of Cd, but not after lesion. After microinjection of naloxone beta-FNA, the specific antagonist for opioid mu receptors, into Cd,the inhibitory effect of EA or activation of Sm I on nociceptive responses of the Pf neurons was abolished, but it was not influenced by microinjection of nor-BNI and ICI174,864, the specific antagonists for opioid kappa and delta receptors, respectively. Together with our previous findings that EA could activate cortical neurons to participate in descending modulation of activities of Pf neurons, the present results suggest that Cd is associated with Sm I generating descending inhibition on nociceptive responses of Pf neurons in AA, and it is most likely that opiates in Cd may be involved in this inhibition through mu but not kappa or delta receptors.
本实验旨在研究尾状核（Cd）是否参与了针刺镇痛（AA）过程中皮层感觉运动区I（Sm I）对束旁核（Pf）产生的下行调制，以及Cd中涉及何种类型的阿片受体。结果发现，在Cd损伤前，电针（EA）和刺激Sm I可抑制Pf神经元的伤害性反应，但损伤后则不能。向Cd内微量注射阿片μ受体特异性拮抗剂纳洛酮β-FNA后，EA或刺激Sm I对Pf神经元伤害性反应的抑制作用消失，但分别向Cd内微量注射阿片κ和δ受体特异性拮抗剂nor-BNI和ICI174,864对此无影响。结合我们之前的研究结果，即EA可激活皮层神经元参与对Pf神经元活动的下行调制，本研究结果表明，Cd与Sm I对AA过程中Pf神经元伤害性反应产生下行抑制有关，且Cd中的阿片类物质很可能通过μ受体而非κ或δ受体参与了这种抑制作用。
