Li M, Rosenberg H C, Chiu T H
Department of Pharmacology, Medical College of Ohio, Toledo 43699-0008.
Eur J Pharmacol. 1993 Nov 15;247(3):313-8. doi: 10.1016/0922-4106(93)90200-s.
The effect of chronic flurazepam treatment on the GABA (gamma-aminobutyric acid) receptor/chloride channel complex was studied using GABA-stimulated 36Cl- influx into brain microsacs, and its potentiation by diazepam, clonazepam and bretazenil. Rats were given flurazepam for 1 week, then microsacs were prepared from cerebral cortices of rats that were still receiving flurazepam, and from those that had stopped treatment 48 h earlier. Diazepam and clonazepam produced concentration-dependent increases in GABA-stimulated 36Cl- influx while bretazenil produced a much smaller effect, which did not reach statistical significance in the tissue from control rats. There was no significant change in the basal or 10 microM GABA-stimulated 36Cl- influx between control and treated groups. Tolerance was shown by a significantly reduced effect of diazepam and clonazepam to enhance GABA-stimulated 36Cl- influx in the tissue prepared from non-withdrawn rats. However, for both diazepam and clonazepam, there was no tolerance 48 h after chronic treatment. The results suggest that changes in the GABA receptor/Cl- channel complex on cerebral cortical neurons contribute to cross-tolerance from flurazepam to other benzodiazepines.
采用γ-氨基丁酸(GABA)刺激36Cl-流入脑微粒体的方法,研究了长期氟西泮治疗对GABA受体/氯离子通道复合物的影响,以及地西泮、氯硝西泮和溴替唑仑对其的增强作用。给大鼠服用氟西泮1周,然后从仍在接受氟西泮治疗的大鼠以及提前48小时停药的大鼠的大脑皮质制备微粒体。地西泮和氯硝西泮使GABA刺激的36Cl-流入呈浓度依赖性增加,而溴替唑仑的作用小得多,在对照组大鼠的组织中未达到统计学显著性。对照组和治疗组之间基础或10μM GABA刺激的36Cl-流入无显著变化。在从未停药的大鼠制备的组织中,地西泮和氯硝西泮增强GABA刺激的36Cl-流入的作用显著降低,表明产生了耐受性。然而,对于地西泮和氯硝西泮,慢性治疗48小时后均未产生耐受性。结果表明,大脑皮质神经元上GABA受体/氯离子通道复合物的变化导致了从氟西泮到其他苯二氮䓬类药物的交叉耐受性。