Lehoullier P F, Ticku M K
Eur J Pharmacol. 1987 Mar 17;135(2):235-8. doi: 10.1016/0014-2999(87)90617-0.
GABAA agonists stimulate 36Cl-influx in spinal cord cultured neurons in a concentration-dependent manner. This effect of GABAA receptor stimulation is enhanced by benzodiazepines like clonazepam, diazepam and flurazepam and attenuated by (+)bicuculline and picrotoxinin. The beta-carbolines, methyl-6, 7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) and propyl-beta-carboline-3-carboxylate (beta-CCPr) exhibited opposite effects, with DMCM attenuating, while beta-CCPr potentiating GABA's effect. These results are consistent with the behavioral and electrophysiological effect of benzodiazepines and beta-carbolines with GABA receptor complex.
GABAA 激动剂以浓度依赖的方式刺激脊髓培养神经元中的 36Cl 内流。像氯硝西泮、地西泮和氟西泮这样的苯二氮䓬类药物可增强 GABAA 受体刺激的这种效应，而（+）荷包牡丹碱和印防己毒素则可减弱该效应。β-咔啉类化合物，甲基-6,7-二甲氧基-4-乙基-β-咔啉-3-羧酸酯（DMCM）和丙基-β-咔啉-3-羧酸酯（β-CCPr）表现出相反的效应，DMCM 减弱而 β-CCPr 增强 GABA 的效应。这些结果与苯二氮䓬类药物和 β-咔啉类化合物对 GABA 受体复合物的行为和电生理效应一致。
