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小鼠中β-咔啉-3-羧酸甲酯诱导惊厥的特征

Characterization of convulsions induced by methyl beta-carboline-3-carboxylate in mice.

作者信息

Prado de Carvalho L, Grecksch G, Cavalheiro E A, Dodd R H, Chapouthier G, Rossier J

出版信息

Eur J Pharmacol. 1984 Aug 17;103(3-4):287-93. doi: 10.1016/0014-2999(84)90489-8.

Abstract

The convulsive properties of methyl beta-carboline-3-carboxylate (beta-CCM) were evaluated in mice. When injected subcutaneously at a dose of 10 mg/kg beta-CCM induced convulsions in 75% of the mice with a median latency of 2.12 +/- 0.25 min. The CD50 was determined to be about 5 mg/kg. Electroencephalographic recordings showed that convulsions were brief (10 s), of cortical origin and propagating rapidly to the hippocampus. EEG alterations induced by low doses of beta-CCM lasted up to 1 h. The convulsive effect of beta-CCM was compared to that of PTZ. PTZ-induced convulsions occurred with a longer latency (9.26 +/- 1.33 min). beta-CCM and PTZ could act synergistically when injected in non-convulsive doses. When beta-CCM was injected 2-30 min before pentylenetetrazol (PTZ) there was a clear potentiation of the convulsive effect of PTZ. The convulsions induced by beta-CCM were blocked by diazepam (DZ) and by Ro 15-1788. In addition, beta-CCM reversed the sedative effect of a high dose of DZ for more than 30 min. Our results confirm that beta-CCM acts through the BZ receptor and indicate that the effects induced by a single dose of beta-CCM last more than 30 min.

摘要

对小鼠评估了β-咔啉-3-羧酸甲酯(β-CCM)的惊厥特性。以10mg/kg的剂量皮下注射时,β-CCM在75%的小鼠中诱发惊厥,中位潜伏期为2.12±0.25分钟。半数惊厥剂量(CD50)确定为约5mg/kg。脑电图记录显示惊厥短暂(10秒),起源于皮层并迅速传播至海马体。低剂量β-CCM诱发的脑电图改变持续长达1小时。将β-CCM的惊厥作用与戊四氮(PTZ)的惊厥作用进行了比较。PTZ诱发惊厥的潜伏期更长(9.26±1.33分钟)。当以非惊厥剂量注射时,β-CCM和PTZ可协同作用。当在戊四氮(PTZ)前2 - 30分钟注射β-CCM时,PTZ的惊厥作用明显增强。β-CCM诱发的惊厥可被地西泮(DZ)和Ro 15 - 1788阻断。此外,β-CCM使高剂量DZ的镇静作用逆转超过30分钟。我们的结果证实β-CCM通过苯二氮䓬受体起作用,并表明单次剂量β-CCM诱导的作用持续超过30分钟。

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