[Mechanism of the modulation of pain transmission at the subnucleus caudalis of the trigeminal sensory nuclear complex in rabbits].

T Shibutani
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Abstract

The modulation of dental pain transmission at the subnucleus caudalis of the trigeminal sensory nuclear complex (SpVc) was investigated in rabbits in vivo. The superficial layers of SpVc were perfused with artificial cerebrospinal fluid using a push-pull cannula system. Immunoreactive substance P (SP) released into the perfusates following electrical stimulation of the lower incisor pulp was measured. The obtained results were as follows. 1. An increase in the release of SP and [Met5]-enkephalin was observed by the electrical stimulation with 40 V. 2. The increase of SP release following electrical stimulation was inhibited by systemic administration of morphine (10 mg/kg i.v.) or local application of morphine (10(-6) M) to SpVc. The stimulus-evoked SP release was also inhibited by local application of [D-Ala2, Met5]-enkephalinamide (an analog of [Met5]-enkephalin; 10(-4) M). 3. Spontaneous release of serotonin (5-HT) into the perfusates was observed, while that of norepinephrine was not. Tooth pulp stimulation tended to increase the level of 5-HT. Systemic administration of morphine (10 mg/kg i.v.) and electrical stimulation of the nucleus raphe magnus (NRM) significantly enhanced the release of 5-HT. 4. The release of SP evoked by tooth pulp stimulation was inhibited by local application of 5-HT (10(-6)M) and electrical stimulation of NRM. These results suggest that there are two modulatory systems controlling the delivery of the ascending sensory message at the superficial layers of SpVc. One is an intrinsic mechanism associated with the segmental enkephalinergic system, the other is a descending monoaminergic system originating in NRM. It is also suggested that these two systems play an important role in producing the analgesic effect of morphine.

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[兔三叉神经感觉核复合体尾侧亚核疼痛传递的调节机制]。
在家兔体内研究了三叉神经感觉核复合体(SpVc)尾侧亚核对牙痛传递的调节。采用推拉式套管系统向SpVc浅层灌注人工脑脊液。测定电刺激下切牙牙髓后向灌注液中释放的免疫反应性物质P (SP)。所得结果如下:1. 用40v . 2电刺激观察SP和[Met5]-脑啡肽的释放增加。全身注射吗啡(10 mg/kg静脉注射)或局部注射吗啡(10(-6)M)可抑制电刺激后SP释放的增加。局部应用[D-Ala2, Met5]-脑啡肽([Met5]-脑啡肽类似物;10(-4) m)。观察到5-羟色胺(5-HT)自发释放到灌注液中,而去甲肾上腺素则没有。牙髓刺激有增加5-HT水平的趋势。全身给药吗啡(10mg /kg静脉注射)和电刺激中缝大核(NRM)显著增强5-HT的释放。4. 局部应用5-HT (10(-6)M)和NRM电刺激可抑制牙髓刺激引起的SP释放。这些结果表明,在SpVc的表层,有两个调节系统控制着上行感觉信息的传递。一个是与节段性脑啡能系统相关的内在机制,另一个是源于NRM的下降单胺能系统。这也表明这两个系统在吗啡镇痛作用的产生中起着重要作用。
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