Eur J Pharmacol. 2013 Nov 15;720(1-3):131-7. doi: 10.1016/j.ejphar.2013.10.036.
In vitro studies show that the abused inhalant toluene affects a number of ligand-gated ion channels.The two most consistently implicated of these are γ-aminobutyric acid type A(GABAA) receptors which are positively modulated by toluene and N-methyl-D-aspartate(NMDA) receptors which are negatively modulated by toluene. Behavioral studies also suggest an interaction of toluene with GABAA and/or NMDA receptors but it is unclear if these receptors underlie the abuse-related intoxicating effects of toluene. Seventeen B6SJLF1/J mice were trained using a two-choice operant drug discrimination procedure to discriminate 10 min of exposure to 2000 ppm toluene vapor from 10 min of exposure to air. The discrimination was acquired in a mean of 65 training sessions. The stimulus effects of 2000 ppm toluene vapor were exposure concentration-dependent but rapidly diminished following the cessation of vapor exposure. The stimulus effects of toluene generalized to the chlorinated hydrocarbon vapor perchloroethylene but not 1,1,2-trichloroethane nor the volatile anesthetic isoflurane. The competitive NMDA antagonist CGS-19755, the uncompetitive antagonist dizocilpine and the glycine-site antagonist L701,324 all failed to substitute for toluene. The classical nonselective benzodiazepines midazolam and chlordiazepoxide produced toluene-like stimulus effects but the alpha 1 subunit preferring positive GABAA modulator zaleplon failed to substitute for toluene. The barbiturates pentobarbital and methohexital and the GABAA positive modulator neurosteroid allopregnanolone did not substitute for toluene. These data suggest that the stimulus effects of toluene may be at least partially mediated by benzodiazepine-like positive allosteric modulation of GABAA receptors containing alpha 2, 3 or 5 subunits.
体外研究表明,滥用吸入剂甲苯会影响多种配体门控离子通道。这些通道中最常涉及的两种是γ-氨基丁酸 A(GABAA)受体,甲苯对其具有正调制作用,而 N-甲基-D-天冬氨酸(NMDA)受体则受到甲苯的负调制作用。行为研究也表明甲苯与 GABAA 和/或 NMDA 受体相互作用,但尚不清楚这些受体是否是甲苯与滥用相关的中毒作用的基础。17 只 B6SJLF1/J 小鼠通过双选择操作性药物辨别程序进行训练,以辨别 10 分钟暴露于 2000 ppm 甲苯蒸气与 10 分钟暴露于空气之间的差异。平均在 65 次训练课程中获得辨别能力。2000 ppm 甲苯蒸气的刺激作用与暴露浓度有关,但在蒸气暴露停止后迅速减弱。甲苯的刺激作用可概括为氯化碳蒸气全氯乙烯,但不能概括为 1,1,2-三氯乙烷或挥发性麻醉剂异氟烷。竞争性 NMDA 拮抗剂 CGS-19755、非竞争性拮抗剂地卓西平(dizocilpine)和甘氨酸部位拮抗剂 L701,324 均未能替代甲苯。经典的非选择性苯二氮䓬类药物咪达唑仑(midazolam)和地西泮(chlordiazepoxide)产生与甲苯相似的刺激作用,但 α1 亚基优先的正 GABAA 调节剂扎来普隆(zaleplon)未能替代甲苯。巴比妥类药物戊巴比妥(pentobarbital)和甲己炔巴比妥(methohexital)以及 GABAA 正调节剂神经甾体 allopregnanolone 均未能替代甲苯。这些数据表明,甲苯的刺激作用至少部分是通过包含 α2、3 或 5 亚基的苯二氮䓬类药物正变构调制 GABAA 受体介导的。