Suppr超能文献

奥卡西平对猫三叉神经脊髓束核记录的牙髓诱发电位的抑制作用。

Suppressive effects of oxcarbazepine on tooth pulp-evoked potentials recorded at the trigeminal spinal tract nucleus in cats.

作者信息

Kiguchi S, Ichikawa K, Kojima M

机构信息

Pharmacology Laboratory, Kissei Pharmaceutical Co. Ltd, Minamiazumi, Nagano, Japan.

出版信息

Clin Exp Pharmacol Physiol. 2001 Mar;28(3):169-75. doi: 10.1046/j.1440-1681.2001.03431.x.

Abstract
  1. The purpose of the present study was to evaluate the antinociceptive effect of oxcarbazepine, a keto derivitive of carbamazepine (an anticonvulsant), in an animal model. To evoke a nociceptive response, we electrically stimulated the maxillary canine tooth pulp (MCTP) in anaesthetized (allobarbital-urethane), spontaneously breathing cats. 2. The evoked potentials were recorded from the superficial layers of the caudal part of the trigeminal spinal tract nucleus (5ST). We examined a slow component with a large amplitude (the P3 component) in evoked compound potentials; its mean conduction velocity was 1.7 m/s, suggesting a response mediated by C-fibres. 3. To confirm that the P3 component was related to pain sensation, we used morphine, a most efficacious antinociceptive agent, in the present study. The P3 component was significantly suppressed by intravenous administration of morphine (3 mg/kg) and was also suppressed by microinjection of morphine (2 microg) into the recording site of the 5ST. These results suggest that the P3 component is involved in the transmission of nociceptive information. 4. We compared the effect of oxcarbazepine with mexiletine; both are known to block neuronal Na+ channels. Intravenous administration of mexiletine suppressed the P3 component at a dose of 5 mg/kg. Microinjection of mexiletine (10 microg) into the recording site of the 5ST tended to suppress the P3 component, but this effect was not significant. 5. Intravenous administration of oxcarbazepine (1-10 mg/kg) caused a dose-dependent inhibition of the P3 component, which was significantly suppressed at 10 mg/kg oxcarbazepine. Intravenous administration of 10,11-dihydro-10-hydroxy-5H-dibenz[b,f]azepine-5-carboxamide (MHD), a metabolite of oxcarbazepine, at doses of 3-30 mg/kg caused a dose-dependent inhibition of the P3 component. Oxcarbazepine was not available for the microinjection study because it is not water soluble. We used MHD for the microinjection study instead of oxcarbazepine, because MHD can be dissolved in water up to 3 mg/mL. Microinjections of MHD (6 microg) into the recording site of the 5ST suppressed the P3 component. These results indicate that oxcarbazepine has an antinociceptive action.
摘要
  1. 本研究的目的是在动物模型中评估奥卡西平(卡马西平(一种抗惊厥药)的酮衍生物)的抗伤害感受作用。为引发伤害性反应,我们在麻醉(异戊巴比妥-乌拉坦)、自主呼吸的猫身上电刺激上颌犬牙髓(MCTP)。2. 从三叉神经脊髓束核(5ST)尾部的表层记录诱发电位。我们在诱发复合电位中检测到一个大振幅的慢成分(P3成分);其平均传导速度为1.7 m/s,提示该反应由C纤维介导。3. 为证实P3成分与痛觉相关,在本研究中我们使用了吗啡(一种最有效的抗伤害感受剂)。静脉注射吗啡(3 mg/kg)可显著抑制P3成分,向5ST记录部位微量注射吗啡(2 μg)也可抑制该成分。这些结果表明P3成分参与伤害性信息的传递。4. 我们比较了奥卡西平与美西律的作用;已知二者均能阻断神经元Na+通道。静脉注射美西律5 mg/kg可抑制P3成分。向5ST记录部位微量注射美西律(10 μg)倾向于抑制P3成分,但该作用不显著。5. 静脉注射奥卡西平(1 - 10 mg/kg)可引起P3成分的剂量依赖性抑制,奥卡西平10 mg/kg时P3成分被显著抑制。静脉注射奥卡西平的代谢产物10,11 - 二氢 - 10 - 羟基 - 5H - 二苯并[b,f]氮杂卓 - 5 - 甲酰胺(MHD),剂量为3 - 30 mg/kg时可引起P3成分的剂量依赖性抑制。由于奥卡西平不溶于水,无法用于微量注射研究。我们使用MHD替代奥卡西平进行微量注射研究,因为MHD可溶于水,浓度可达3 mg/mL。向5ST记录部位微量注射MHD(6 μg)可抑制P3成分。这些结果表明奥卡西平具有抗伤害感受作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验