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急性给予利血平会引发长期的自发性口腔运动障碍。

Acute reserpine administration elicits long-term spontaneous oral dyskinesia.

作者信息

Sussman A N, Tran-Nguyen L T, Neisewander J L

机构信息

Department of Psychology, Arizona State University, Tempe 85287-1104, USA.

出版信息

Eur J Pharmacol. 1997 Oct 22;337(2-3):157-60. doi: 10.1016/s0014-2999(97)01271-5.

Abstract

Chronic reserpine administration produces persistent oral dyskinesia accompanied by severe dopamine depletion in the caudate-putamen. The present study examined whether these behavioral and neurochemical effects would persist following acute reserpine administration. Acute administration of reserpine (1 mg/kg, s.c.) produced spontaneous oral dyskinesia that persisted above control levels for at least 84 days. Reserpine also produced a 74% depletion of dopamine in the caudate-putamen relative to vehicle treatment at 3 days post-injection, but did not significantly alter dopamine in the caudate-putamen at 84 days post-injection. The finding that reserpine-induced oral dyskinesia persisted despite repletion of dopamine in the caudate-putamen suggests that the persistent neuropathological change underlying this behavior occurs in a neural pathway other than the dopaminergic nigrostriatal pathway.

摘要

长期给予利血平会导致持续性口腔运动障碍,并伴有尾状核 - 壳核中严重的多巴胺耗竭。本研究考察了急性给予利血平后,这些行为和神经化学效应是否会持续存在。急性给予利血平(1毫克/千克,皮下注射)会产生自发性口腔运动障碍,该障碍在至少84天内持续高于对照水平。相对于注射后3天的溶剂处理,利血平还使尾状核 - 壳核中的多巴胺耗竭了74%,但在注射后84天,并未显著改变尾状核 - 壳核中的多巴胺水平。尽管尾状核 - 壳核中的多巴胺已恢复,但利血平诱导的口腔运动障碍仍持续存在,这一发现表明,这种行为背后持续的神经病理变化发生在多巴胺能黑质纹状体通路以外的神经通路中。

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