D1多巴胺受体的激活会刺激大鼠基底神经节中γ-氨基丁酸（GABA）的释放。

Activation of D1 dopamine receptors stimulates the release of GABA in the basal ganglia of the rat.

作者信息

Floran B, Aceves J, Sierra A, Martinez-Fong D

机构信息

Department of Physiology, Biophysics and Neurosciences, Instituto Politecnico Nacional, Mexico, D.F.

出版信息

Neurosci Lett. 1990 Aug 14;116(1-2):136-40. doi: 10.1016/0304-3940(90)90399-t.

DOI:10.1016/0304-3940(90)90399-t

PMID:2147981

Abstract

Here we have explored whether dopamine is able to modulate the release of gamma-aminobutyric acid (GABA) from striatal terminals to substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and caudate-putamen. The type of dopamine receptors involved was assessed by the blocking effect of either SCH 23390 (D1 antagonist) or (-)-sulpiride (D2 antagonist) of the dopamine effect. Dopamine stimulated (EC50 3.2 microM) the depolarization-induced release of [3H]GABA from slices isolated from all of the above mentioned nuclei. SCH 23390 dose-dependently blocked the dopamine stimulation, but (-)-sulpiride did not show any blocking effect. The results suggest that dopamine via D1 receptors modulates the release of GABA from striatal GABAergic terminals.

摘要

在此，我们探究了多巴胺是否能够调节从纹状体终末到黑质网状部、内苍白球核、苍白球和尾状核 - 壳核的γ - 氨基丁酸（GABA）释放。通过SCH 23390（D1拮抗剂）或（ - ） - 舒必利（D2拮抗剂）对多巴胺效应的阻断作用来评估所涉及的多巴胺受体类型。多巴胺刺激（EC50为3.2微摩尔）了从上述所有核分离的切片中去极化诱导的[3H]GABA释放。SCH 23390剂量依赖性地阻断了多巴胺刺激，但（ - ） - 舒必利未显示出任何阻断作用。结果表明，多巴胺通过D1受体调节来自纹状体GABA能终末的GABA释放。