在利血平处理的小鼠中,可乐定对多巴胺依赖性运动的增强作用仅限于D2激动剂。

M S Starr, B S Starr
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引用次数: 12

摘要

小鼠给予利血平(5mg /kg), 24h后完全无动力学反应。D1选择性激动剂SKF 38393 (3-30 mg/kg IP)、D2选择性激动剂RU 24213 (0.5-5 mg/kg SC)和D1/D2混合激动剂阿波啡(0.025-0.5 mg/kg SC)恢复流畅运动。可乐定(0.03125-1 mg/kg IP)对多巴胺完整小鼠有剂量依赖性镇静作用,但对单胺缺失小鼠的运动活性无影响。在药物相互作用实验中,可乐定没有改变SKF 38393的运动刺激作用,但大大增强了对RU 24213和阿波啡的运动反应。这些结果支持了一种假设,即在利血平治疗的帕金森病小鼠模型中,α -肾上腺素能受体激动剂促进多巴胺D2而不是多巴胺D1运动反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Potentiation of dopamine-dependent locomotion by clonidine in reserpine-treated mice is restricted to D2 agonists.

Mice treated with reserpine (5 mg/kg IP), 24 h beforehand, were completely akinetic. Fluent locomotion was reinstated with the D1-selective agonist SKF 38393 (3-30 mg/kg IP), the D2-selective agonist RU 24213 (0.5-5 mg/kg SC) and the mixed D1/D2 agonist apomorphine (0.025-0.5 mg/kg SC). Clonidine (0.03125-1 mg/kg IP) caused a dose-dependent sedation in dopamine-intact mice, but had no effect by itself on the locomotor activity of monoamine-depleted mice. In drug interaction experiments, clonidine did not modify the motor stimulant action of SKF 38393, but greatly enhanced the motor responses to RU 24213 and apomorphine. These results support the hypothesis that alpha-adrenoceptor agonists facilitate dopamine D2 but not dopamine D1 motor responding in the reserpine-treated mouse model of Parkinson's disease.

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