Narihara R, Hirouchi M, Ichida T, Kuriyama K, Roberts E
Department of Pharmacology, Kyoto Prefectural University of Medicine, Japan.
Neurochem Int. 1994 Nov;25(5):451-4. doi: 10.1016/0197-0186(94)90021-3.
The effects of thyroxine and its related derivatives on gamma-aminobutyric acid (GABA) receptors in the rat brain were examined. D-Thyroxine strongly inhibited [3H]flunitrazepam binding to benzodiazepine receptor in crude synaptic membrane from the rat brain. The Scatchard analysis of the [3H]flunitrazepam binding in the presence of D-thyroxine indicated the decreases in the affinity and maximum number of binding site. Furthermore, D-thyroxine inhibited the enhancing effect of flunitrazepam on GABA-stimulated 36Cl- influx into membrane vesicles, although GABA-stimulated 36Cl- influx alone was not affected by D-thyroxine. On the other hand, the effects of thyroxine and its related derivatives on cerebral GABAB receptor binding were not noted. These results suggest that D-thyroxine may be a drug which is able to modulate the function of GABAA receptor complex via the inhibitory action on benzodiazepine recognition site.
研究了甲状腺素及其相关衍生物对大鼠脑内γ-氨基丁酸（GABA）受体的影响。D-甲状腺素强烈抑制[3H]氟硝西泮与大鼠脑粗制突触膜中苯二氮䓬受体的结合。对存在D-甲状腺素时[3H]氟硝西泮结合进行的Scatchard分析表明，结合位点的亲和力和最大数量均降低。此外，D-甲状腺素抑制了氟硝西泮对GABA刺激的36Cl-流入膜囊泡的增强作用，尽管单独的GABA刺激的36Cl-流入不受D-甲状腺素影响。另一方面，未观察到甲状腺素及其相关衍生物对脑GABAB受体结合的影响。这些结果表明，D-甲状腺素可能是一种能够通过对苯二氮䓬识别位点的抑制作用来调节GABAA受体复合物功能的药物。
