Matsumoto Norio, Fukuda Daisuke, Murata Junichiro, Yamada Hiroyuki, Miura Hiroyuki, Kitada Yasuyuki
Department of Oral Physiology, School of Dentistry, Iwate Medical University, Chuoh-dori 1-3-27, Morioka, Iwate 020-8505, Japan.
Arch Oral Biol. 2006 Oct;51(10):930-9. doi: 10.1016/j.archoralbio.2006.04.005. Epub 2006 Jun 13.
Internal capsule (IC) stimulation has been used clinically to alleviate central pain. However, the neuronal mechanisms underlying pain relief by IC stimulation are poorly understood. In order to elucidate the analgesic mechanism, the effect of IC conditioning stimulation on nociceptive neurons in the rat medullary dorsal horn was investigated in the present study. Rats were anaesthetized with N(2)O-O(2) (2:1) and 0.5% halothane and were immobilized with pancuronium bromide. Two kinds of nociceptive neurons, wide dynamic range (WDR) and nociceptive specific (NS) neurons, responding to noxious stimulations of the face and oral structures were recorded in the trigeminal caudal nucleus and the medial reticular subnuclei. A test stimulus with a single rectangular pulse (2ms in duration, 5-70V) was applied to the centre of the receptive field. Responses in 55.9% of the WDR neurons and in 60% of the NS neurons were inhibited by conditioning stimuli to the ipsilateral IC with trains of 33 pulses (100-300microA) at 330Hz. The percents of peak inhibitory effects on WDR neurons and NS neurons were 78.1+/-25.0% (n=19) and 89.0+/-13.6% (n=3), respectively. The inhibitory effect continued for conditioning-test intervals of up to 500ms. Effective sites for conditioning stimulation were concentrated in the lateral side of the IC. These findings suggest that modulation of nociceptive transmission by IC stimulation occurs at second-order neurons via a presynaptic phenomenon by corticofugal fibers in the IC.
内囊(IC)刺激已在临床上用于缓解中枢性疼痛。然而,IC刺激缓解疼痛的神经元机制尚不清楚。为了阐明镇痛机制,本研究探讨了IC条件刺激对大鼠延髓背角伤害性神经元的影响。大鼠用N₂O - O₂(2:1)和0.5%氟烷麻醉,并用泮库溴铵固定。在三叉神经尾核和内侧网状亚核中记录了两种对脸部和口腔结构的伤害性刺激有反应的伤害性神经元,即广动力范围(WDR)神经元和伤害性特异(NS)神经元。将一个持续2毫秒、5 - 70伏的单个矩形脉冲测试刺激施加到感受野中心。通过以330赫兹施加33个脉冲(100 - 300微安)的串刺激同侧IC,55.9%的WDR神经元和60%的NS神经元的反应受到抑制。对WDR神经元和NS神经元的峰值抑制效应百分比分别为78.1±25.0%(n = 19)和89.0±13.6%(n = 3)。抑制效应在条件刺激 - 测试间隔长达500毫秒时持续存在。条件刺激的有效部位集中在内囊的外侧。这些发现表明,IC刺激对伤害性传递的调制是通过内囊中皮质下行纤维的突触前现象在二级神经元处发生的。