Simmonds M A
Eur J Pharmacol. 1985 Oct 29;117(1):51-60. doi: 10.1016/0014-2999(85)90471-6.
In slices of rat cuneate nucleus, responses to the GABA-A receptor agonist muscimol were potentiated by flurazepam. The maximal potentiation by 1 microM flurazepam was antagonized by the neuronal benzodiazepine receptor ligand Ro15-1788 3 microM, by the quinoline derivative PK8165 0.1 microM and by the peripheral-type benzodiazepine receptor ligand Ro5-4864 0.1 microM. Another ligand for the peripheral-type benzodiazepine receptor, PK11195 10 microM, enhanced the potentiating effect of a submaximal concentration of flurazepam 0.1 microM and prevented the antagonism of flurazepam by Ro5-4864. At much higher concentrations of these drugs, additional effects were seen. Ro15-1788 30 microM and PK11195 30 microM each caused small potentiations of muscimol while Ro5-4864 30 microM caused a small antagonism. Ro15-1788 30 microM, PK8165 100 microM and Ro5-4864 30 microM all antagonized the potentiation of muscimol by pentobarbitone 10 microM; also, PK8165 and Ro5-4864 enhanced the potency of picrotoxin as an antagonist of muscimol. It is concluded that both Ro5-4864 and PK8165 have several distinct effects on the GABA-A receptor complex, all of which could result in reduced responses to muscimol.
在大鼠楔束核切片中,氟西泮可增强对GABA - A受体激动剂蝇蕈醇的反应。1微摩尔氟西泮的最大增强作用可被3微摩尔的神经元苯二氮䓬受体配体Ro15 - 1788、0.1微摩尔的喹啉衍生物PK8165以及0.1微摩尔的外周型苯二氮䓬受体配体Ro5 - 4864所拮抗。外周型苯二氮䓬受体的另一种配体10微摩尔的PK11195,增强了0.1微摩尔亚最大浓度氟西泮的增强作用,并阻止了Ro5 - 4864对氟西泮的拮抗作用。在这些药物浓度更高时,还可见到其他效应。30微摩尔的Ro15 - 1788和30微摩尔的PK11195各自对蝇蕈醇产生轻微增强作用,而30微摩尔的Ro5 - 4864则产生轻微拮抗作用。30微摩尔的Ro15 - 1788、100微摩尔的PK8165和30微摩尔的Ro5 - 4864均拮抗了10微摩尔戊巴比妥对蝇蕈醇的增强作用;此外,PK8165和Ro5 - 4864增强了印防己毒素作为蝇蕈醇拮抗剂的效力。得出的结论是,Ro5 - 4864和PK8165对GABA - A受体复合物均有几种不同的作用,所有这些作用都可能导致对蝇蕈醇的反应降低。