Porceddu M L, Giorgi O, Ongini E, Mele S, Biggio G
Life Sci. 1986 Jul 28;39(4):321-8. doi: 10.1016/0024-3205(86)90650-8.
Chronic treatment with SCH 23390, a selective D-1 dopamine receptor antagonist, elicited a 32% increase in the density of 3H-SCH 23390 binding sites in nigral membrane preparations but failed to change the apparent KD of the ligand for its binding sites. Haloperidol, a D-2 dopamine receptor antagonist which blocks the dopamine-sensitive adenylate cyclase and (-) sulpiride, a selective D-2 dopamine receptor blocker, which does not block the dopamine-sensitive adenylate cyclase, failed to change both the Bmax and KD of 3H-SCH 23390 binding. Finally, the intrastriatal injection of kainic acid produced a marked decrease of both GAD activity and GABA content and 3H-SCH 23390 binding sites (65%) in the homolateral substantia nigra. The results show that in the rat substantia nigra most of the 3H-SCH 23390 binding sites have a presynaptic localization on the striato-nigral GABAergic afferent terminals and suggest that dopamine released from nigral dendrites exerts a tonic influence on these presynaptic D-1 dopamine receptors.
用选择性D-1多巴胺受体拮抗剂SCH 23390进行长期治疗，可使黑质膜制剂中3H-SCH 23390结合位点的密度增加32%，但未能改变配体与其结合位点的表观解离常数（KD）。能阻断多巴胺敏感性腺苷酸环化酶的D-2多巴胺受体拮抗剂氟哌啶醇以及不阻断多巴胺敏感性腺苷酸环化酶的选择性D-2多巴胺受体阻滞剂（-）舒必利，均未能改变3H-SCH 23390结合的最大结合容量（Bmax）和解离常数（KD）。最后，纹状体内注射 kainic 酸可使同侧黑质中的谷氨酸脱羧酶（GAD）活性、γ-氨基丁酸（GABA）含量以及3H-SCH 23390结合位点显著减少（65%）。结果表明，在大鼠黑质中，大多数3H-SCH 23390结合位点位于纹状体-黑质γ-氨基丁酸能传入终末的突触前部位，并提示从黑质树突释放的多巴胺对这些突触前D-1多巴胺受体发挥着紧张性影响。
