Nagatani T, Yamamoto T, Sugihara T, Ueki S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Jpn J Pharmacol. 1988 Mar;46(3):267-74. doi: 10.1254/jjp.46.267.
The effect of anxiolytics, benzodiazepine (BZP), diazepam (DZP), non-BZP zopiclone (ZOP) and phenobarbital (PBT), on the proconflict effect induced by methyl-beta-carboline-3-carboxylate (beta-CCM) or by pentetrazol (PTZ) was investigated. The proconflict effect of beta-CCM and PTZ was reduced by these anxiolytics and aminooxyacetic acid (AOAA). In addition, isoniazid produced proconflict activity. Therefore, it is suggested that anxiolytics facilitate the GABA-ergic function, causing the inhibition of the proconflict effect. Although both propyl-beta-carboline-3-carboxylate (beta-CCP) and Ro15-1788 did not produce proconflict activity, they reduced the proconflict effect induced by beta-CCM but not by PTZ. These data clearly show that beta-CCM exerts the proconflict effect through interaction with BZP receptor and that there are behavioral similarities between beta-CCP and Ro15-1788. In this study, we additionally observed the time latency until the rat began to drink the water. beta-CCM and PTZ prolonged this latency in a dose-dependent manner. However, AOAA could not reduce the prolonged latency induced by beta-CCM and by PTZ, and anxiolytics and beta-CCP could not reduce the prolonged latency induced by beta-CCM. The mechanism of the prolongation of latency induced by beta-CCM and PTZ seems to be different from that of the proconflict effect.
研究了抗焦虑药苯二氮䓬(BZP)、地西泮(DZP)、非苯二氮䓬类的佐匹克隆(ZOP)和苯巴比妥(PBT)对由甲基-β-咔啉-3-羧酸(β-CCM)或戊四氮(PTZ)诱导的促冲突效应的影响。这些抗焦虑药和氨氧基乙酸(AOAA)可降低β-CCM和PTZ的促冲突效应。此外,异烟肼产生促冲突活性。因此,提示抗焦虑药促进γ-氨基丁酸(GABA)能功能,从而抑制促冲突效应。虽然丙基-β-咔啉-3-羧酸(β-CCP)和Ro15-1788均未产生促冲突活性,但它们可降低由β-CCM诱导而非由PTZ诱导的促冲突效应。这些数据清楚地表明,β-CCM通过与苯二氮䓬受体相互作用发挥促冲突效应,且β-CCP与Ro15-1788之间存在行为学相似性。在本研究中,我们还观察了大鼠开始饮水前的潜伏时间。β-CCM和PTZ以剂量依赖的方式延长了该潜伏时间。然而,AOAA不能缩短由β-CCM和PTZ诱导的延长的潜伏时间,抗焦虑药和β-CCP也不能缩短由β-CCM诱导的延长的潜伏时间。β-CCM和PTZ诱导潜伏时间延长的机制似乎与促冲突效应的机制不同。