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首页> 外文期刊>Japanese Journal of Pharmacology >Selective Blockade of Dopamine D-1 Receptor by SCH 23390 Affects Dopamine Agonist Binding to 3H-Spiperone Labeled D-2 Receptors in Rat Striatum
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Selective Blockade of Dopamine D-1 Receptor by SCH 23390 Affects Dopamine Agonist Binding to 3H-Spiperone Labeled D-2 Receptors in Rat Striatum

机译:SCH 23390对多巴胺D-1受体的选择性阻断影响多巴胺激动剂与大鼠纹状体中3H-Spiperone标记的D-2受体的结合

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References(40) Cited-By(6) This study investigated the effects of selective blockade of dopamine D-1 receptors by SCH 23390 and selective stimulation of the receptors by SKF 38393 on the binding characteristics of 3H-spiperone labeled D-2 receptors in rat striatum. Selective blockade of D-1 receptors by 50 nM SCH 23390 significantly decreased the affinity of dopamine agonist for 3H-spiperone labeled D-2 receptors, but did not influence dopamine antagonist binding to D-2 receptors. Selective stimulation of D-1 receptors by SKF 38393 (100 nM) did not affect either dopamine agonist or antagonist binding to D-2 receptors. The characteristics of the effect of SCH 23390 on dopamine agonist binding to D-2 receptors was similar to those of GTP, but different from those of sodium ion. This effect could not be due to a direct modification of D-2 receptors by SCH 23390. Pertussis toxin (IAP) treatment significantly decreased the affinity of dopamine agonist for D-2 receptors and reduced the abilities of both SCH 23390 and GTP to decrease the affinity of dopamine agonist for D-2 receptors. These results suggest, therefore, putative interregulatory mechanism between dopamine D-1 and D-2 receptors and the possible involvement of a pertussis toxin sensitive protein in this mechanism.
机译:参考文献(40)Cited-By(6)该研究研究了SCH 23390对多巴胺D-1受体的选择性阻断和SKF 38393对该受体的选择性刺激对3H-哌啶酮标记的D-2受体结合特性的影响。大鼠纹状体。 50 nM SCH 23390对D-1受体的选择性阻断显着降低了多巴胺激动剂对3H-哌啶酮标记的D-2受体的亲和力,但不影响多巴胺拮抗剂与D-2受体的结合。 SKF 38393(100 nM)对D-1受体的选择性刺激不影响多巴胺激动剂或拮抗剂与D-2受体的结合。 SCH 23390对多巴胺受体激动剂与D-2受体结合的作用与GTP相似,但与钠离子不同。这种作用可能不是由于SCH 23390对D-2受体的直接修饰。百日咳毒素(IAP)处理显着降低了多巴胺激动剂对D-2受体的亲和力,并降低了SCH 23390和GTP降低D-2受体的能力。多巴胺激动剂对D-2受体的亲和力。因此,这些结果表明,多巴胺D-1和D-2受体之间可能存在相互调节的机制,百日咳毒素敏感蛋白可能参与了这种机制。

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