GABA(B)-RECEPTOR-MEDIATED INHIBITION OF CALCIUM SIGNALS IN ISOLATED NERVE-TERMINALS

被引：10

作者：

TAREILUS, E ^{[1
]}

SCHOCH, J ^{[1
]}

BREER, H ^{[1
]}

机构：

[1] UNIV STUTTGART HOHENHEIM, INST ZOOPHYSIOL, D-70593 STUTTGART, GERMANY

来源：

NEUROCHEMISTRY INTERNATIONAL | 1994年 / 24卷 / 04期

关键词：

D O I：

10.1016/0197-0186(94)90113-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Time-resolved fluorometric monitoring of rapid changes in intracellular Ca2+-concentrations [Ca2+](i) was employed to analyze the effect of gamma-aminobutyric acid (GABA) on evoked Ca2+-signals in rat hippocampal synaptosomes. The inhibitory action of GABA was mimicked by Baclofen, the selective agonist for GABA(B)-receptors, and also by the nonhydrolyzable GTP-derivalive CTP-gamma-S. Preincubation of synaptosomes with GABA or baclofen for up to 250 ms before depolarization resulted in a maximal inhibition. The GABA-induced attenuation of the evoked rise in [Ca2+](i) was maximal during the first milliseconds after depolarization. The inhibitory action of GABA apparently does not involve second messengers, such as cAMP or IP3/DAG; the GABA-induced inhibition of presynaptic voltage-dependent Ca2+-channels may be mediated directly by G-proteins.

引用

页码：349 / 361

页数：13

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