Cerebral Acetylcholine in Thiamine Deficiency 1
Cerebral Acetylcholine in Thiamine Deficiency 1
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硫胺素缺乏症中的脑乙酰胆碱 1
DOI：
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发表时间：
1970
期刊：
影响因子：
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通讯作者：
S. Schenker
中科院分区：
文献类型：
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作者：
K. Speeg;D. Chen;D. McCandless;S. Schenker
总结本研究评估的假设，严重的硫胺素缺乏症可能会导致大脑乙酰胆碱，这反过来，可能是负责在这种情况下看到的脑功能障碍耗尽。在饮食诱导的硫胺素缺乏导致明显神经系统体征的大鼠和无症状的成对喂养和正常喂养对照组中进行乙酰胆碱测定。除皮质外，还对脑干和小脑进行了分析，因为前者在硫胺素缺乏时表现出最显著的生化改变。乙酰胆碱的测定是通过一个特定的和准确的荧光法的修改。对于每一个脑区研究硫胺素缺乏大鼠表现出明显的神经症状的脑乙酰胆碱浓度相比，在无症状的配对喂养对照组中看到的值。这项研究表明，硫胺素缺乏症不会导致改变大脑区域乙酰胆碱储存和神经功能障碍的替代机制将不得不寻求。
Summary This study assesses the hypothesis that severe thiamine deficiency may lead to a depletion of cerebral ACh, which, in turn, may be responsible for the cerebral dysfunction seen in this condition. Acetylcholine assays were carried out in rats with diet-induced thiamine deficiency resulting in overt neurologic signs and in asymptomatic pair-fed and normally fed controls. The brainstem and cerebellum were assayed, in addition to the cortex, since the former sites exhibit the most significant biochemical alterations in thiamine deficiency. Acetylcholine was assayed by a modification of a specific and accurate fluorometric procedure. For every brain area studied the cerebral ACh concentrations in thiamine-deficient rats exhibiting overt neurologic signs were comparable to values seen in asymptomatic pair-fed controls. This study indicates that thiamine deficiency does not cause an alteration in cerebral regional ACh stores and that alternate mechanisms for the neurologic dysfunction will have to be sought.