Klockgether T, Schwarz M, Turski L, Sontag K H
Eur J Pharmacol. 1985 Apr 16;110(3):309-15. doi: 10.1016/0014-2999(85)90557-6.
ZK 91296, a newly synthesised beta-carboline with partial agonistic activity at the benzodiazepine receptor raised the threshold current necessary to elicit electroconvulsions in mice. This effect was dose-dependent and could be reversed by Ro 15-1788. ZK 91296 antagonised the anticonvulsant action of diazepam, but potentiated that of phenobarbitone. ZK 91296 protected mice from DMCM-induced seizures with high potency, this effect being benzodiazepine specific. In mutant rats exhibiting an increased muscle tone of the hindlimbs, ZK 91296 was devoid of muscle relaxant effect and antagonised the muscle relaxant action of both diazepam and phenobarbitone. The latter effect could be blocked by Ro 15-1788. The results suggest that the actions of ZK 91296 are only partly due to its partial agonistic properties at the benzodiazepine receptor.
ZK 91296是一种新合成的β-咔啉，对苯二氮䓬受体具有部分激动活性，它提高了诱发小鼠惊厥所需的阈电流。这种效应呈剂量依赖性，且可被Ro 15 - 1788逆转。ZK 91296拮抗地西泮的抗惊厥作用，但增强苯巴比妥的抗惊厥作用。ZK 91296能高效保护小鼠免受DMCM诱导的惊厥，这种效应具有苯二氮䓬特异性。在表现出后肢肌张力增加的突变大鼠中，ZK 91296没有肌肉松弛作用，且拮抗地西泮和苯巴比妥的肌肉松弛作用。后一种效应可被Ro 15 - 1788阻断。结果表明，ZK 91296的作用仅部分归因于其对苯二氮䓬受体的部分激动特性。
