Abramets I I, Komissarov I V
Biull Eksp Biol Med. 1984 Jun;97(6):679-81.
Experiments on an isolated spinal cord of 8-15-day-old rats have shown that one of the possible mechanisms of the GABA-potentiating action of the benzodiazepine tranquilizer, chlorodiazepoxide, may be a decrease in the intraneuronal concentration of Ca2+. This is evidenced by the enhancement of the GABA-potentiating action of chlorodiazepoxide under Ca2+ deficiency in the medium and in the presence of the blockers of the voltage-dependent Ca2+ ionic channels--Mn2+ and Co2+, and by the reduction of the effect in question under Ca2+ excess in the medium and in the presence of the K+ channels blockers--tetraethylammonium and 4-aminopyridine. The GABA-potentiating action of harmane is likely to be related to the blockade of the voltage-dependent K+ channels and elevation of the intracellular concentration of Ca2+.
对8至15日龄大鼠的离体脊髓进行的实验表明,苯二氮䓬类镇静剂氯氮卓增强γ-氨基丁酸(GABA)作用的一种可能机制可能是神经元内钙离子(Ca2+)浓度降低。培养基中缺乏Ca2+以及存在电压依赖性Ca2+离子通道阻滞剂锰离子(Mn2+)和钴离子(Co2+)时氯氮卓增强GABA的作用增强,而培养基中Ca2+过量以及存在钾离子(K+)通道阻滞剂四乙铵和4-氨基吡啶时该作用减弱,这些均证明了这一点。哈尔满增强GABA的作用可能与阻断电压依赖性K+通道及提高细胞内Ca2+浓度有关。