Role of D1 receptor mechanisms in the potentiation of motor responses to L-dopa and apomorphine by MK 801 in the reserpine-treated mouse.

S Kaur, M S Starr, B S Starr
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引用次数: 11

Abstract

In 24 h reserpine-treated akinetic mice, locomotion was induced by the D1-selective agonist SKF 38393 (30 mg/kg IP), or by the mixed D1/D2 agonists L-dopa (150 mg/kg IP, plus benserazide 100 mg/kg IP) and apomorphine (0.5 mg/kg SC). The non-competitive NMDA receptor antagonist MK 801 (0.01-1.6 mg/kg IP) did not induce motor activity by itself, but potentiated the motor responses to L-dopa and apomorphine at roughly 10-fold lower doses than those which facilitated D1 responding. These data cast doubt on the notion that glutamate antagonists enhance the antiparkinsonian efficacy of mixed D1/D2 agonists solely through a D1 receptor mechanism.

D1受体机制在利血平处理小鼠MK 801增强左旋多巴和阿波啡运动反应中的作用。
利血平处理24 h后,D1选择性激动剂SKF 38393 (30 mg/kg IP)或D1/D2混合激动剂左旋多巴(150 mg/kg IP,加苯沙肼100 mg/kg IP)和阿波啡(0.5 mg/kg SC)诱导运动。非竞争性NMDA受体拮抗剂MK 801 (0.01 ~ 1.6 mg/kg IP)本身不诱导运动活动,但增强了左旋多巴和阿波啡的运动反应,其剂量比促进D1反应的剂量低约10倍。这些数据对谷氨酸拮抗剂仅通过D1受体机制增强混合D1/D2激动剂抗帕金森病疗效的观点提出了质疑。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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