Expósito I, Del Arco A, Segovia G, Mora F
Department of Physiology, Faculty of Medicine, University Complutense, Madrid, Spain.
Neurochem Res. 1999 Jul;24(7):849-56. doi: 10.1023/a:1020901929419.
Interactions between endogenous dopamine, glutamate, GABA, and taurine were investigated in striatum of the freely moving rat by using microdialysis. Intrastriatal infusions of the selective dopamine uptake inhibitor nomifensine (NMF) were used to increase the endogenous extracellular dopamine. NMF produced a dose-related increase in extracellular dopamine and also increased extracellular concentrations of glutamate, GABA, and taurine. Extracellular increases of dopamine were significantly correlated with extracellular increases of glutamate and GABA, but not taurine. To investigate whether the increased extracellular dopamine produced by NMF was responsible for the concomitant increase of glutamate and GABA, D1, and D2 receptor antagonists were used. Dopamine receptor antagonists D1 (SCH23390) and D2 (sulpiride) significantly attenuated the increases of glutamate and GABA produced by NMF. These data suggest that endogenous dopamine, through both D1 and D2 dopamine receptors, plays a role in releasing glutamate and GABA in striatum of the freely moving rat.
通过微透析技术,研究了自由活动大鼠纹状体内内源性多巴胺、谷氨酸、γ-氨基丁酸(GABA)和牛磺酸之间的相互作用。纹状体内注射选择性多巴胺摄取抑制剂诺米芬辛(NMF)以增加内源性细胞外多巴胺。NMF使细胞外多巴胺呈剂量依赖性增加,同时也使谷氨酸、GABA和牛磺酸的细胞外浓度升高。多巴胺的细胞外增加与谷氨酸和GABA的细胞外增加显著相关,但与牛磺酸无关。为了研究NMF产生的细胞外多巴胺增加是否导致谷氨酸和GABA的同时增加,使用了D1和D2受体拮抗剂。多巴胺受体拮抗剂D1(SCH23390)和D2(舒必利)显著减弱了NMF引起的谷氨酸和GABA增加。这些数据表明,内源性多巴胺通过D1和D2多巴胺受体,在自由活动大鼠纹状体内释放谷氨酸和GABA中发挥作用。