Neuman R S, Thompson P M
Faculty of Medicine, Memorial University, St. John's, Newfoundland, Canada.
Epilepsia. 1989 May-Jun;30(3):307-13. doi: 10.1111/j.1528-1157.1989.tb05302.x.
Noxious stimulation can suppress epileptic seizures in humans and epileptiform activity in laboratory animals. Using as a model system the focal epileptiform activity (FEA) induced by the pneumophoresis of penicillin, the role of 5-hydroxytryptamine (5HT) in suppression of this activity by noxious stimulation was investigated. Drugs known to depress dorsal raphe unit activity, (+/-)-8-hydroxydipropylaminotetralin (DPAT), imipramine, and fluoxetine prevented suppression of FEA induced by noxious stimulation. Desimipramine, which depresses locus ceruleus but not dorsal raphe unit activity, was ineffective in blocking the suppression. Quipazine, an agonist at 5-HT receptors, in part restored the suppression that had been blocked by DPAT or imipramine. Several serotonin antagonists effective at 5-HT1 and 5-HT2 receptors blocked suppression, but an unequivocal determination of the serotonin receptor subtype mediating suppression could not be made. We conclude that 5-HT mediates suppression of FEA induced by noxious stimulation.
伤害性刺激能够抑制人类的癫痫发作以及实验动物的癫痫样活动。以青霉素透入法诱发的局灶性癫痫样活动（FEA）作为模型系统，研究了5-羟色胺（5HT）在伤害性刺激抑制该活动中的作用。已知能抑制中缝背核单位活动的药物，（±）-8-羟基二丙基氨基四氢萘（DPAT）、丙咪嗪和氟西汀可阻止伤害性刺激对FEA的抑制作用。去甲丙咪嗪可抑制蓝斑核但不影响中缝背核单位活动，它在阻断抑制作用方面无效。5-羟色胺受体激动剂喹哌嗪部分恢复了被DPAT或丙咪嗪阻断的抑制作用。几种对5-HT1和5-HT2受体有效的5-羟色胺拮抗剂可阻断抑制作用，但无法明确介导抑制作用的5-羟色胺受体亚型。我们得出结论，5-HT介导伤害性刺激对FEA的抑制作用。
