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In vivo imaging of dopaminergic neurotransmission after transient focal ischemia in rats

机译:大鼠短暂性局灶性局部缺血后多巴胺能神经传递的体内成像

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摘要

The precise biologic mechanisms involved in functional recovery processes in response to stroke such as dopaminergic neurotransmission are still largely unknown. For this purpose, we performed in parallel in vivo magnetic resonance imaging and positron emission tomography (PET) with [18F]fluorodeoxyglucose ([18F]FDG) and [11C]raclopride at 1, 3, 7, 14, 21, and 28 days after middle cerebral artery occlusion in rats. In the ischemic territory, PET [18F]FDG showed a initial decrease in cerebral metabolism followed by a time-dependent recovery to quasi-normal values at day 14 after ischemia. The PET with [11C]raclopride, a ligand for dopamine D2 receptor, showed a sustained binding during the first week after ischemia that declined dramatically from day 14 to day 28. Interestingly, a slight increase in [11C]raclopride binding was observed at days 1 to 3 followed by the uppermost binding at day 7 in the contralateral territory. Likewise, in vitro autoradiography using [3H]raclopride confirmed these in vivo results. Finally, the neurologic test showed major neurologic impairment at day 1 followed by a recovery of the cerebral function at day 28 after cerebral ischemia. Taken together, these results might suggest that dopamine D2 receptor changes in the contralateral hemisphere could have a key role in functional recovery after cerebral ischemia.
机译:关于中风例如多巴胺能神经传递的功能恢复过程所涉及的确切生物学机制仍是未知的。为此,我们使用[ 18 F]氟脱氧葡萄糖([ 18 F] FDG)和[ sup> 11 C] raclopride在大鼠大脑中动脉闭塞后的第1、3、7、14、21和28天。在缺血区域,PET [ 18 F] FDG表现出脑代谢的初步下降,随后在缺血后第14天随时间恢复至准正常值。具有[ 11 C]雷氯必利(一种多巴胺D2受体的配体)的PET在缺血后的第一周显示出持续的结合,从第14天到第28天急剧下降。有趣的是,[在对侧区域中,在第1至3天观察到 11 C] raclopride结合,然后在第7天观察到最高结合。同样,使用[ 3 H]雷氯必利的体外放射自显影证实了这些体内结果。最后,神经系统检查显示在脑缺血后第1天出现严重的神经功能障碍,然后在第28天恢复了脑功能。综上所述,这些结果可能表明对侧半球中的多巴胺D2受体变化可能在脑缺血后的功能恢复中起关键作用。

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