PARADOXICAL KINESIA IN PARKINSONISM IS NOT CAUSED BY DOPAMINE RELEASE - STUDIES IN AN ANIMAL-MODEL
PARADOXICAL KINESIA IN PARKINSONISM IS NOT CAUSED BY DOPAMINE RELEASE - STUDIES IN AN ANIMAL-MODEL
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DOI：
10.1001/archneur.1989.00520460046012
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发表时间：
1989-10-01
影响因子：
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通讯作者：
STRICKER, EM
中科院分区：
文献类型：
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作者：
KEEFE, KA;SALAMONE, JD;STRICKER, EM
在大量多巴胺耗竭的脑损伤后，大鼠变得行动不灵，但它们表现出激活诱导的运动功能恢复。在这项研究中，大鼠被给予脑室注射神经毒素6-羟基多巴胺，以永久性地减少纹状体中的多巴胺含量98%。尽管这些老鼠在家中的笼子里动弹不得，但当它们被放入深水中时，它们可以有效地游泳，并从浅水漂浮的冰浴中逃脱。用多巴胺拮抗剂氟哌啶醇和SCH-23390对动物进行预处理并不能消除这些行为。相比之下，氟哌啶醇完全阻断了大脑受损动物对苯丙胺的行为反应。这些结果表明，多巴胺耗竭大鼠的矛盾运动不是从残留的多巴胺能纤维中释放多巴胺的结果。
Rats become akinetic after large dopamine-depleting brain lesions, yet they show an activation-induced restoration of motor function. In this study, rats were given intraventricular injections of the neurotoxin 6-hydroxydopamine to permanently reduce the dopamine content of the corpus striatum by 98%. Although the rats were akinetic in their home cages, they swam effectively when placed in deep water and escaped from a shallow floating ice bath. These behaviors were not abolished by pretreating the animals with the dopamine antagonists haloperidol and SCH-23390. In contrast, haloperidol completely blocked the brain-damaged animals'' behavioral responses to amphetamine. These results suggest that the paradoxical kinesia of dopamine-depleted rats is not a consequence of dopamine release from residual dopaminergic fibers.