Behavioral and neurochemical alterations following thiamine deficiency in rodents: relationship to functions of cholinergic neurons.
Behavioral and neurochemical alterations following thiamine deficiency in rodents: relationship to functions of cholinergic neurons.
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DOI：
10.1248/yakushi.125.549
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发表时间：
2005-07
期刊：
影响因子：
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通讯作者：
O. Nakagawasai
中科院分区：
文献类型：
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作者：
O. Nakagawasai
在硫胺素缺乏（TD）喂养的后期（20-25天）诱导记忆缺陷。本文就胆碱能神经元在TD喂养所致记忆障碍中的作用作一综述。虽然记忆缺陷不能抑制注射硫胺素，一旦出现，这种损害被认为是保护早期治疗与硫胺素在TD喂养。给药毒蕈碱M（1）激动剂McN-A-343可逆转TD小鼠的记忆缺陷，但毒蕈碱M（2）拮抗剂methoctramine不能。“汉方”（传统草药）药物“kami-untan-to”（KUT）可防止在TD小鼠中观察到的记忆缺陷。胆碱乙酰转移酶（ChAT）荧光强度是胆碱能神经元突触前的标志，在TD早期（第14天）在皮层和海马降低，在TD晚期（第25天）在大范围脑区降低。早期KUT治疗抑制TD小鼠海马中ChAT的减少。提示TD早期胆碱能功能下降可能是导致记忆障碍的原因，胆碱能神经元的激活可能在TD记忆障碍的改善中起重要作用。
Memory deficits are induced during the late stage (20-25 days) of thiamine-deficient (TD) feeding. In this review, the role of cholinergic neurons on the memory deficit induced by TD feeding are summarized. Although memory deficit cannot be suppressed by an injection of thiamine once it appears, such impairment was found to be protected by early treatment with thiamine during TD feeding. Administration of muscarinic M(1) agonist McN-A-343 reversed the memory deficit observed in TD mice, although the muscarinic M(2) antagonist methoctramine did not. The "kampo" (traditional herbal) medicine, "kami-untan-to" (KUT), protected against the memory deficit observed in TD mice. Choline acetyltransferase (ChAT) fluorescence intensity, a marker of presynapse of cholinergic neurons, was decreased in the cortex and hippocampus at an early stage (14th day) of TD, and it was decreased in a wide range of brain areas at a late stage (25th day) of TD. Early KUT treatment inhibited the reduction of ChAT in the hippocampus of TD mice. These findings suggested that the memory deficit may be caused by a reduction in the cholinergic function at an early stage of TD, and that the activation of cholinergic neurons may play an important role in the improvement of TD-induced memory deficit.