Brennan M J
J Neurochem. 1982 Jan;38(1):264-6. doi: 10.1111/j.1471-4159.1982.tb10879.x.
Depolarization-induced release of [3H]gamma-aminobutyric acid ([3H]-GABA) from preloaded slices of rat cerebral cortex was inhibited by muscimol and THIP in a dose-dependent fashion. This inhibition of release was prevented by the GABA antagonists bicuculline and picrotoxin. These results confirm previous reports postulating the existence of GABA autoreceptors on GABAergic terminals. Since benzodiazepines are known to facilitate post-synaptic GABA actions, the effect of flunitrazepam on the inhibition of GABA release mediated through the autoreceptors has been examined. At a concentration of 1 microM or 10 microM, flunitrazepam had no effect on the IC50 values for muscimol or THIP in inhibiting stimulated GABA release. It thus seems that GABA autoreceptors are not functionally coupled to benzodiazepine receptors in rat cerebral cortex.
在预先装载的大鼠大脑皮层切片中,去极化诱导的[³H]γ-氨基丁酸([³H]-GABA)释放受到蝇蕈醇和四氢异喹啉的剂量依赖性抑制。GABA拮抗剂荷包牡丹碱和苦味毒可阻止这种释放抑制。这些结果证实了先前关于GABA能终末上存在GABA自身受体的报道。由于已知苯二氮䓬类药物可促进突触后GABA作用,因此研究了氟硝西泮对通过自身受体介导的GABA释放抑制的影响。在1微摩尔或10微摩尔的浓度下,氟硝西泮对蝇蕈醇或四氢异喹啉抑制刺激的GABA释放的IC50值没有影响。因此,在大鼠大脑皮层中,GABA自身受体似乎在功能上不与苯二氮䓬受体偶联。