Gajendiran M, Seth P, Ganguly D K
Division of Pharmacology and Experimental Therapeutics, Indian Institute of Chemical Biology, Jadavpur, Calcutta, India.
Neuroreport. 1996 Jan 31;7(2):513-6. doi: 10.1097/00001756-199601310-00033.
The relative roles of D1 and D2 dopamine (DA) receptors in mediating apomorphine (APO)-induced changes in the spinal reflex was investigated. Low doses of APO, a DA receptor agonist (0.2 mg kg-1, i.v.), depressed the monosynaptic mass reflex (MMR) in spinalized rats. Pretreatment with the D2-specific antagonist, spiperone, 10 min before APO prevented the APO-induced MMR depression. Pretreatment with the D1 antagonist SCH 23390 failed to prevent the APO-induced depression. Interestingly, SCH 23390 pretreatment preferentially antagonized the depression induced by a high dose of APO (3 mg kg-1, i.v.). Pretreatment with SKF 38393, a selective D1 agonist, completely prevented the APO-induced MMR depression. These results suggest that inhibition of spinal transmission by low dose of APO may be mediated through its action on presynaptic D2 receptors and that D1 and D2 receptors are functionally coupled at the spinal level in modulating the spinal motor output.
研究了D1和D2多巴胺（DA）受体在介导阿扑吗啡（APO）诱导的脊髓反射变化中的相对作用。低剂量的DA受体激动剂阿扑吗啡（0.2 mg/kg，静脉注射）可抑制脊髓大鼠的单突触群体反射（MMR）。在阿扑吗啡给药前10分钟用D2特异性拮抗剂螺哌隆预处理可防止阿扑吗啡诱导的MMR抑制。用D1拮抗剂SCH 23390预处理未能防止阿扑吗啡诱导的抑制。有趣的是，SCH 23390预处理优先拮抗高剂量阿扑吗啡（3 mg/kg，静脉注射）诱导的抑制。用选择性D1激动剂SKF 38393预处理可完全防止阿扑吗啡诱导的MMR抑制。这些结果表明，低剂量阿扑吗啡对脊髓传递的抑制可能是通过其对突触前D2受体的作用介导的，并且D1和D2受体在调节脊髓运动输出方面在脊髓水平上功能耦合。
