Blanchet P J, Konitsiotis S, Chase T N
Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-1406, USA.
Mov Disord. 1998 Sep;13(5):798-802. doi: 10.1002/mds.870130507.
The antidyskinetic potential of the glutamate NMDA receptor channel blocker amantadine was evaluated in four levodopa-primed parkinsonian monkeys using two different regimens (1.25 or 2.5 mg/kg administered subcutaneously twice daily for 3-6 days). When administered with a relatively low dose of levodopa, amantadine produced a near-total suppression of choreiform dyskinesias and a substantial reduction in dystonic dyskinesias at the expense of a significant reduction in antiparkinsonian response. With a high dose of levodopa, amantadine had a smaller but still significant effect on dyskinesias without altering the antiparkinsonian response. These results lend support to the view that glutamate receptor-mediated mechanisms contribute to levodopa-induced dyskinesias. They also suggest that amantadine could alleviate such complications in parkinsonian patients, especially with careful dose optimization.
在四只左旋多巴预处理的帕金森病猴中,使用两种不同方案(每天皮下注射1.25或2.5mg/kg,持续3 - 6天)评估了谷氨酸N-甲基-D-天冬氨酸(NMDA)受体通道阻滞剂金刚烷胺的抗运动障碍潜力。当与相对低剂量的左旋多巴合用时,金刚烷胺几乎完全抑制了舞蹈样运动障碍,并显著减少了张力障碍性运动障碍,但代价是抗帕金森病反应显著降低。使用高剂量的左旋多巴时,金刚烷胺对运动障碍的影响较小但仍显著,且不改变抗帕金森病反应。这些结果支持了谷氨酸受体介导的机制导致左旋多巴诱导的运动障碍这一观点。它们还表明,金刚烷胺可以减轻帕金森病患者的此类并发症,尤其是通过仔细优化剂量。