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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Physostigmine reversal of scopolamine-induced hypofrontality.
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Physostigmine reversal of scopolamine-induced hypofrontality.

机译：东pol碱引起的低剂量的地斯的明的逆转。

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The muscarinic receptor antagonist scopolamine produces a transient memory deficit in healthy humans. This deficit has been offered as a model of the cholinergic deficit of Alzheimer's disease (AD). However, we have previously shown that scopolamine produces a deficit of cortical perfusion maximal in the frontal lobe, dissimilar to the parietal cortex deficit characteristic of AD. The current experiment was aimed at replicating and extending this observation by critically testing the central cholinergic origin of both cognitive and perfusion deficits. Nine healthy subjects participated in regional cerebral blood flow (rCBF) measurements at baseline, after scopolamine (7.2 micrograms/kg i.v.), and after both physostigmine (22 micrograms/kg i.v.) and neostigmine (7 or 11 micrograms/kg i.v.). rCBF was quantified by the xenon 133 inhalation method. As expected, scopolamine reduced cortical perfusion, mainly in the frontal cortex, and produced a memory deficit. Physostigmine, but not neostigmine, reversed all three variables partially or completely. These results support the hypothesis that all three consequences of scopolamine, namely, reduction of mean flow, frontal deficit, and memory impairment, are cholinergically mediated. Furthermore, because neostigmine poorly crosses the blood-brain barrier, these findings confirm that the effect is centrally mediated and cannot be explained by peripheral effects. However, they also confirm the frontal cortex locus of action for both scopolamine and its reversal by physostigmine and therefore suggest a major dissimilarity to the characteristic rCBF appearance of AD. This study extends our previous preliminary findings with tacrine and strengthens the suggestion that only nicotinic receptors are associated with the characteristic parietal deficit of AD.
机译：毒蕈碱受体拮抗剂东pol碱在健康的人类中会产生短暂的记忆障碍。该缺陷已作为阿尔茨海默氏病（AD）胆碱能缺乏的模型提供。但是，我们以前已经证明东pol碱会在额叶中产生最大的皮质灌注不足，这与AD的顶叶皮质缺乏特性不同。当前的实验旨在通过严格测试认知缺陷和灌注缺陷的中心胆碱能起源来复制和扩展这一观察结果。 9名健康受试者在基线时，东pol碱（7.2微克/千克静脉），以及毒扁豆碱（22微克/千克静脉）和新斯的明（7或11微克/千克静脉）的基线时参加了局部脑血流量（rCBF）的测量。 rCBF通过氙133吸入法定量。如所料，东pol碱可减少主要在额叶皮层的皮质灌注，并产生记忆障碍。毒扁豆碱而非新斯的明可部分或完全逆转所有三个变量。这些结果支持以下假设：东pol碱的所有三种后果，即平均流量减少，额叶赤字和记忆力减退均由胆碱介导。此外，由于新斯的明很难很好地穿过血脑屏障，因此这些发现证实该作用是集中介导的，不能用外周作用来解释。但是，他们也证实了东pol碱的前额皮质运动位点以及毒扁豆碱的逆转作用，因此表明与AD的特征性rCBF外观存在重大差异。这项研究扩展了我们以前使用他克林的初步发现，并加强了仅烟碱样受体与AD的特征性顶叶赤字相关的建议。

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