Department of Pharmacology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr.-mail code 7764, San Antonio, TX 78229-3900, USA.
Eur J Pharmacol. 2013 Jan 30;700(1-3):159-64. doi: 10.1016/j.ejphar.2012.12.028. Epub 2013 Jan 7.
Benzodiazepines and neuroactive steroids act at distinct binding sites on γ-aminobutyric acid(A) (GABA(A)) receptors where they positively modulate GABA, resulting in similar acute behavioral effects. Tolerance to benzodiazepines can develop with repeated treatment; however, cross tolerance to neuroactive steroids does not develop, perhaps due to conformational changes in benzodiazepine, and not neuroactive steroid, binding sites. Three monkeys discriminated 0.178 mg/kg midazolam while responding under a fixed-ratio 10 schedule of stimulus-shock termination. On separate occasions, dose-effect curves for midazolam and pregnanolone were determined when monkeys had not received chlordiazepoxide and when they received 10 mg/kg chlordiazepoxide 46 hours earlier; for some tests, flumazenil was given before determination of dose-effect curves. Midazolam and pregnanolone produced ≥80% midazolam-lever responding. When administered 46 h before sessions, chlordiazepoxide did not produce pregnanolone-lever responding; under those treatment conditions, midazolam dose-effect curves were shifted 2.8-fold rightward and pregnanolone dose-effect curves were not changed. Flumazenil antagonized midazolam; Schild (linear) analyses yielded slopes that were not different from unity and pA(2) values of 7.46 when monkeys had not received chlordiazepoxide and 7.44 when they received chlordiazepoxide 46 h earlier. Flumazenil did not alter the effects of pregnanolone in chlordiazepoxide-treated monkeys. Thus, interactions between flumazenil and midazolam were not qualitatively or quantitatively changed in monkeys acutely tolerant to chlordiazepoxide, suggesting that mechanisms other than alterations of benzodiazepine binding sites account for the development of acute tolerance.
苯二氮䓬类药物和神经活性甾体在γ-氨基丁酸(GABA(A))受体的不同结合部位起作用,它们正向调节 GABA,导致类似的急性行为效应。反复治疗可产生苯二氮䓬类药物的耐受性;然而,神经活性甾体不会产生交叉耐受性,这可能是由于苯二氮䓬类药物结合部位的构象变化,而不是神经活性甾体结合部位的构象变化。三只猴子在固定比率 10 的刺激-终止条件下,对 0.178 mg/kg 的咪达唑仑做出辨别反应。在不同的情况下,当猴子没有接受地西泮和接受 10 mg/kg 地西泮 46 小时前,确定咪达唑仑和孕烷醇酮的剂量-效应曲线;在一些测试中,在确定剂量-效应曲线之前给予氟马西尼。咪达唑仑和孕烷醇酮产生≥80%的咪达唑仑杠杆反应。在治疗 46 小时前给药时,地西泮不会产生孕烷醇酮杠杆反应;在这些治疗条件下,咪达唑仑剂量-效应曲线向右移动 2.8 倍,而孕烷醇酮剂量-效应曲线没有变化。氟马西尼拮抗咪达唑仑;Schild(线性)分析得到的斜率与单位没有差异,当猴子没有接受地西泮时,pA(2)值为 7.46,当它们接受地西泮 46 小时前,pA(2)值为 7.44。氟马西尼在接受地西泮治疗的猴子中没有改变孕烷醇酮的作用。因此,在急性对地西泮耐受的猴子中,氟马西尼和咪达唑仑之间的相互作用在质量或数量上没有改变,这表明急性耐受的发展除了改变苯二氮䓬类药物结合部位外,还有其他机制。