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丘脑束旁核 (PF)被认为是痛觉整合的高级中枢。大量实验资料证实蓝斑 (LC)通过其NE能下行纤维末梢在脊髓背角中阻断痛信号的传递。新近用行为法测痛的资料表明鞘内注入K+ATP通道激动剂和腺苷可引起镇痛。本实验利用乌拉坦麻醉的Wistar大鼠 ,采用常规细胞外放电技术 ,记录PF神经元伤害性放电作为背角中痛信号传递过程受调制的指标 ,观察刺激蓝斑结合鞘内注入K+ATP通道阻断剂优降糖 (Gli)和激动剂Nicoradil(Nic)以及腺苷阻断剂氨茶碱 (Aph)和激动剂NECA对LC刺激效应的影响。结果显示 :①蓝斑刺激可明显抑制外周强电流刺激 (或夹尾 )诱发的PF神经元的伤害性放电 ,抑制百分率为 (84± 17.7) % (n =10 ) ;②鞘内注入K+ATP通道阻断剂Gli(10nmol/L)或腺苷阻断剂Aph (12 0nmol/L)均可取消蓝斑刺激引起的PF神经元痛放电的抑制 ;③鞘内注入K+ATP通道激动剂Nic(0 .3nmol/L)或腺苷激动剂NECA(1nmol/L)均可抑制PF的伤害性痛放电 ,抑制百分率分别为 (83.2± 2 0 ) %和 (88.7± 11) % ;④鞘内注入Aph能取消鞘内Nic引起的伤害性放电的抑制 ,而鞘内Gli不能取消NECA引起的伤害性放电的抑制。上述结果可得出如下推论 :①腺苷和K+ATP通道介导了蓝斑刺激引起的脊髓水平痛信号传递的抑制 ;②可能的作用模式是蓝斑刺激引起了NE?
Thalamic parafascicular nucleus (PF) is considered to be the superior center of analgesia. Numerous experimental data confirm that locus luteus (LC) blocks the transmission of pain signals in the dorsal horn of the spinal cord through its NE-descending fiber terminals. Recent data from behavioral pain tests indicate that intrathecal injection of K + ATP channel agonists and adenosine can cause analgesia. In this study, urethane anesthetized Wistar rats were used to record PF neuronal nociceptive discharge as an indicator of pain signal transmission in the dorsal horn. Conventional extracellular discharge technique was used to observe the effects of stimulation of locus coeruleus injection into K + ATP channel The effect of Gli and Nicoradil (Nic) and adenosine blockers Aph and Agonist NECA on LC stimulatory effects. The results showed that: (1) Plaque stimulation significantly inhibited the noxious discharge of PF neurons induced by peripheral strong current stimulation (or nip), the percentage of inhibition was (84 ± 17.7)% (n = 10) ATP channel blocker Gli (10nmol / L) or adenosine blocker Aph (120nmol / L) could both inhibit the inhibition of PF neuronal pain discharge induced by locus coeruleus. ③Injection of K + ATP channel agonist The nocturnal discharges of PF were inhibited by Nic (0.3 nmol / L) or adenosine (NECA) (1 nmol / L), with the percentages of inhibition being (83.2 ± 20)% and (88.7 ± 11) Intrathecal injection of Aph suppresses the inhibition of nociceptive discharge caused by intrathecal Nic, whereas intrathecal Gli can not abrogate the inhibition of NECA-induced nociceptive discharge. The above conclusions can be deduced as follows: (1) adenosine and K + ATP channels mediate the inhibition of spinal cord pain signal transmission caused by locus coeruleus; (2) the possible mode of action is locus coeruleus