Aceves J, Floran B, Martinez-Fong D, Benitez J, Sierra A, Flores G
Departamento de Fisiologia, Biofisica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Mexico, Mexico.
Neurosci Lett. 1992 Sep 28;145(1):40-2. doi: 10.1016/0304-3940(92)90198-g.
D1 dopamine receptors are present on terminals of striatal neurons to the pars reticulata of the substantia nigra in the rat. Here we have studied the effect of the activation of these receptors on the synthesis of gamma-aminobutyric acid (GABA) in slices of the pars reticulata of the substantia nigra isolated from 6-hydroxydopamine-lesioned rats. The synthesis was judged by the accumulation of GABA after inhibiting GABA transaminase with aminooxyacetic acid. Both dopamine and SCH 23390, a D1 agonist, stimulated the synthesis. The effect of both compounds was blocked by SCH 23390, a D1 antagonist, but not by sulpiride, a D2 antagonist. In the absence of receptor activation, the synthesis was very slow. The results suggest a trophic influence of dopamine upon the synthesis of GABA via D1 receptors.
D1多巴胺受体存在于大鼠黑质网状部纹状体神经元的终末上。在此，我们研究了激活这些受体对从6-羟基多巴胺损伤大鼠分离出的黑质网状部切片中γ-氨基丁酸（GABA）合成的影响。通过用氨氧基乙酸抑制GABA转氨酶后GABA的积累来判断合成情况。多巴胺和D1激动剂SCH 23390均刺激了合成。两种化合物的作用均被D1拮抗剂SCH 23390阻断，但未被D2拮抗剂舒必利阻断。在没有受体激活的情况下，合成非常缓慢。结果表明多巴胺通过D1受体对GABA的合成具有营养作用。
