Nagatani T, Yamamoto T, Takao K, Sugihara T, Ueki S
Department of Pharmacology, Asahi Chemical Ind. Co., Ltd., Miyazaki, Japan.
Jpn J Pharmacol. 1990 Mar;52(3):441-7. doi: 10.1254/jjp.52.441.
Intravenous administration of beta-CCM (methyl-beta-carboline-3-carboxylate) at doses ranging from 0.3 to 10 mg/kg dose-dependently inhibited muricide in olfactory bulbectomized rats. beta-CCM elicited a decrease of locomotor activity at doses ranging from 0.3 to 3 mg/kg, and it impaired rotarod performance at doses of 1 and 3 mg/kg. The inhibition of muricide induced by beta-CCM was antagonized by intraperitoneal administration of Ro15-1788 at 10 mg/kg or diazepam at 3 mg/kg. However, the hypolocomotor activity and impairment of rotarod performance induced by beta-CCM were not antagonized by diazepam at 3 mg/kg. These results indicated that beta-CCM exerts an inhibitory effect on muricide through benzodiazepine receptors and this inhibitory effect was not solely caused by its sedative or motor incordinating activity at the dose ranges used in this study.
以0.3至10毫克/千克的剂量静脉注射β-CCM(甲基-β-咔啉-3-羧酸盐)可剂量依赖性地抑制嗅球切除大鼠的杀鼠行为。β-CCM在0.3至3毫克/千克的剂量范围内引起运动活动减少,并且在1和3毫克/千克的剂量下损害转棒试验表现。腹腔注射10毫克/千克的Ro15-1788或3毫克/千克的地西泮可拮抗β-CCM诱导的杀鼠行为抑制。然而,3毫克/千克的地西泮不能拮抗β-CCM诱导的运动活动减少和转棒试验表现损害。这些结果表明,β-CCM通过苯二氮䓬受体对杀鼠行为发挥抑制作用,并且在本研究使用的剂量范围内,这种抑制作用并非仅由其镇静或运动协调活性引起。