Santiago M, Machado A, Cano J
Departamento de Bioquimica, Facultad de Farmacia, Sevilla, Spain.
Eur J Pharmacol. 1993 Aug 3;239(1-3):83-91. doi: 10.1016/0014-2999(93)90979-r.
The effect of dopamine D1 and D2 receptors agonists and antagonists on extracellular dopamine release was evaluated by microdialysis in the prefrontal cortex. Nomifensine (5 microM) was included in the Ringer solution during the experiments. Cortical dopamine release was tetrodotoxin- and calcium-dependent and was stimulated by high potassium (60 mM) Ringer solution. 1-Methyl-4-phenylpyridinium ion (MPP+) (10 mM) increased the extracellular output of dopamine. SKF-38393 decreased the release of dopamine in a dose-related manner to about 80, 40 and 0% of the control values at 0.1, 1 and 10 microM, respectively. The decrease produced by SKF-38393 (10 microM) was partially antagonized by SCH-23390 at a concentration of 1 microM. Perfusion of CY-208243 (10 microM) produced a decrease in the release of dopamine to about 70% of controls. Quinpirole, at a concentration of 10 microM, produced a decrease in the release of dopamine to about 65% of controls. SCH-23390 and sulpiride, at 10 microM, increased the extracellular output of dopamine to about 150% of controls. These results indicate that dopamine D1 and D2 receptors are implicated in the autoregulation of dopamine release in the prefrontal cortex.
通过微透析法评估多巴胺D1和D2受体激动剂与拮抗剂对前额叶皮质细胞外多巴胺释放的影响。实验过程中，林格液中加入了诺米芬辛（5微摩尔）。皮质多巴胺释放依赖于河豚毒素和钙，并受到高钾（60毫摩尔）林格液的刺激。1-甲基-4-苯基吡啶离子（MPP+）（10毫摩尔）增加了多巴胺的细胞外输出量。SKF-38393以剂量相关的方式降低多巴胺释放，在0.1、1和10微摩尔时分别降至对照值的约80%、40%和0%。SKF-38393（10微摩尔）产生的降低作用在1微摩尔浓度的SCH-23390作用下部分被拮抗。灌注CY-208243（10微摩尔）使多巴胺释放降至对照值的约70%。喹吡罗在10微摩尔浓度时使多巴胺释放降至对照值的约65%。SCH-23390和舒必利在10微摩尔时使多巴胺的细胞外输出量增加至对照值的约150%。这些结果表明，多巴胺D1和D2受体参与前额叶皮质中多巴胺释放的自动调节。
