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γ-氨基丁酸增强钾离子刺激的大鼠黑质和纹状体切片中3H-多巴胺的释放。

GABA potentiates potassium-stimulated 3H-dopamine release from slices of rat substantia nigra and corpus striatum.

作者信息

Starr M S

出版信息

Eur J Pharmacol. 1978 Apr 1;48(3):325-8. doi: 10.1016/0014-2999(78)90091-2.

DOI:10.1016/0014-2999(78)90091-2
PMID:639860
Abstract

GABA (10-5--10-3 M) had no effect on the spontaneous outflow of previously accumulated 3H-DA or 3H-5HT from rat nigral or striatal slices. However, GABA markedly potentiated the potassium-stimulated release of 3H-DA in both brain regions, while the depolarization-induced output of 3H-5HT was only slightly increased. This action of GABA was blocked by pictotoxin but not by bicuculline. Amphetamine likewise evoked a dose-related efflux of 3H-DA and 3H-5HT from nigra and striatum, but these releases were unchanged by GABA. The data suggest that GABA acts presynaptically in these areas to regulate dopaminergic cell function.

摘要

γ-氨基丁酸(10⁻⁵ 至 10⁻³ 摩尔/升)对先前积累在大鼠黑质或纹状体切片中的³H-多巴胺或³H-5-羟色胺的自发流出没有影响。然而,γ-氨基丁酸在这两个脑区均显著增强了钾离子刺激的³H-多巴胺释放,而去极化诱导的³H-5-羟色胺释放仅略有增加。γ-氨基丁酸的这一作用被印防己毒素阻断,但不被荷包牡丹碱阻断。安非他命同样引起³H-多巴胺和³H-5-羟色胺从黑质和纹状体剂量相关的流出,但这些释放不受γ-氨基丁酸影响。数据表明,γ-氨基丁酸在这些区域通过突触前作用来调节多巴胺能细胞功能。

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GABA potentiates potassium-stimulated 3H-dopamine release from slices of rat substantia nigra and corpus striatum.γ-氨基丁酸增强钾离子刺激的大鼠黑质和纹状体切片中3H-多巴胺的释放。
Eur J Pharmacol. 1978 Apr 1;48(3):325-8. doi: 10.1016/0014-2999(78)90091-2.
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Axonal mechanisms mediating γ-aminobutyric acid receptor type A (GABA-A) inhibition of striatal dopamine release.介导γ-氨基丁酸 A 型受体(GABA-A)抑制纹状体多巴胺释放的轴突机制。
Elife. 2020 Sep 1;9:e55729. doi: 10.7554/eLife.55729.
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A Role for Adenosine A1 Receptors in GABA and NMDA-Receptor Mediated Modulation of Dopamine Release: Studies Using Fast Cyclic Voltammetry.
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Br J Pharmacol. 1980 Jan;68(1):162P-163P.
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