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阿扑吗啡或溴隐亭对单突触反射的抑制作用并非由D1/D2受体介导。

Depression of the monosynaptic reflex by apomorphine or bromocriptine is not mediated by D1/D2 receptors.

作者信息

Kamijo N, Nagao T, Ono H

机构信息

Department of Toxicology and Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.

出版信息

Neuropharmacology. 1993 Aug;32(8):777-83. doi: 10.1016/0028-3908(93)90186-7.

Abstract

The role of dopamine in spinal motor transmission was investigated using spinal reflexes in acutely spinalized rats. Intravenous administration of a relatively high dose of the dopamine receptor agonist apomorphine-HCl (3 mg/kg) or the D2 receptor agonist bromocriptine mesylate (1 mg/kg) reduced the amplitude of the monosynaptic reflex (MSR). Depression of the MSR by both drugs was antagonized by haloperidol (1 mg/kg), but not by the D2 receptor antagonists YM-09151-2 (0.2 mg/kg) and sulpiride (10 mg/kg), or by a combination of the D1 receptor antagonist SKF 83566 (0.01 mg/kg) and sulpiride (10 mg/kg). Intravenous administration of the selective D1 receptor agonist SKF 77434 (0.1 and 1 mg/kg) and the D2/D3 receptor agonist quinpirole-HCl (0.1 and 1 mg/kg) had no significant effect on the MSR. Simultaneous administration of SKF 77434 and quinpirole had no significant effect on the MSR. These results show that stimulation of D1/D2 receptors has little influence on the MSR, and suggest that descending dopaminergic systems mediating these receptors have little influence on MSR transmission. Apomorphine and bromocriptine may inhibit the MSR via other subtypes of D1/D2 or other, as yet undiscovered, dopamine receptors or via non-dopaminergic mechanisms.

摘要

利用急性脊髓损伤大鼠的脊髓反射,研究了多巴胺在脊髓运动传递中的作用。静脉注射相对高剂量的多巴胺受体激动剂盐酸阿扑吗啡(3毫克/千克)或D2受体激动剂甲磺酸溴隐亭(1毫克/千克)可降低单突触反射(MSR)的幅度。氟哌啶醇(1毫克/千克)可拮抗这两种药物对MSR的抑制作用,但D2受体拮抗剂YM-09151-2(0.2毫克/千克)和舒必利(10毫克/千克),或D1受体拮抗剂SKF 83566(0.01毫克/千克)与舒必利(10毫克/千克)的组合则不能。静脉注射选择性D1受体激动剂SKF 77434(0.1和1毫克/千克)和D2/D3受体激动剂盐酸喹吡罗(0.1和1毫克/千克)对MSR无显著影响。同时给予SKF 77434和喹吡罗对MSR也无显著影响。这些结果表明,刺激D1/D2受体对MSR影响很小,提示介导这些受体的下行多巴胺能系统对MSR传递影响很小。阿扑吗啡和溴隐亭可能通过D1/D2的其他亚型或其他尚未发现的多巴胺受体,或通过非多巴胺能机制抑制MSR。

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