自身受体调节豚鼠小肠中γ-[³H]氨基丁酸的释放。

Autoreceptors regulate gamma-[3H]aminobutyric acid release from the guinea pig small intestine.

作者信息

Taniyama K, Hanada S, Tanaka C

出版信息

Neurosci Lett. 1985 Apr 9;55(2):245-8. doi: 10.1016/0304-3940(85)90028-x.

Abstract

The possible presence of a presynaptic gamma-aminobutyric acid (GABA) receptor capable of regulating the release of GABA was investigated using the guinea pig small intestine. Muscimol at 10(-8) M and 10(-7) M, but not baclofen at 10(-6) M, inhibited the K+ (40 mM)-evoked Ca2+-dependent release of [3H]GABA from the small intestine preloaded with [3H]GABA, in the presence of 10(-6) M tetrodotoxin. The effect of muscimol on the K+-evoked GABA release was inhibited by bicuculline and furosemide. These results show that the guinea pig small intestine possesses presynaptic GABA receptors which may be involved in the regulation of the evoked GABA release. The presynaptic GABA receptor is bicuculline-sensitive and is probably coupled to the Cl- ion channel.

摘要

利用豚鼠小肠研究了可能存在的能够调节γ-氨基丁酸（GABA）释放的突触前GABA受体。在存在10⁻⁶ M河豚毒素的情况下，10⁻⁸ M和10⁻⁷ M的蝇蕈醇可抑制预先用[³H]GABA加载的小肠中由40 mM K⁺诱发的、依赖Ca²⁺的[³H]GABA释放，但10⁻⁶ M的巴氯芬则无此作用。荷包牡丹碱和速尿可抑制蝇蕈醇对K⁺诱发的GABA释放的作用。这些结果表明，豚鼠小肠具有突触前GABA受体，其可能参与诱发的GABA释放的调节。突触前GABA受体对荷包牡丹碱敏感，可能与Cl⁻离子通道偶联。