Pazo J H, Murer G M, Segal E
Universidad de Buenos Aires, Facultad de Medicina, Departamento de Fisiología, Paraguay, Argentina.
Brain Res Bull. 1993;30(5-6):635-9. doi: 10.1016/0361-9230(93)90094-r.
The role of D1 and D2 striatal dopamine receptors on circling behavior was studied in a normosensitive model obtained by unilateral kainic acid lesion of the entopeduncular nucleus. In this model, the sensitivity of striatal dopamine receptors was preserved, because kainic acid destroyed the neurons of the entopeduncular nucleus and left undamage the fibers of passage and axon terminals. Systemic administration of SKF 38393 to these animals fails to induce circling activity. In contrast, administration of quinpirole elicited rotation toward the lesioned side, which was increased by concurrent injection of SKF 38393. This behavior was inhibited by pretreatment with either a specific D1 (SCH 23390) or D2 (-sulpiride) antagonist. The apomorphine also induced ipsilateral circling that was abolished by pretreatment with D1 or D2 antagonists. The above results suggest that coactivation of both D1 and D2 striatal dopamine receptors are necessary to induce rotation in this normosensitive model.
在通过内苍白球单侧注射海藻酸损伤获得的正常敏感模型中，研究了D1和D2纹状体多巴胺受体在转圈行为中的作用。在该模型中，纹状体多巴胺受体的敏感性得以保留，因为海藻酸破坏了内苍白球的神经元，而未损伤传导纤维和轴突终末。对这些动物全身给予SKF 38393未能诱导出转圈活动。相反，给予喹吡罗可引起向损伤侧旋转，同时注射SKF 38393可增强这种旋转。这种行为可被特异性D1拮抗剂（SCH 23390）或D2拮抗剂（舒必利）预处理所抑制。阿扑吗啡也诱导同侧转圈，D1或D2拮抗剂预处理可消除这种转圈。上述结果表明，在该正常敏感模型中，D1和D2纹状体多巴胺受体的共同激活对于诱导旋转是必需的。
