지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
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Objectives : Besides of malnutrition and neurotoxic effect of alcohol on the prefrontal cortex or subcortical structures, premature aging may be involved in alcohol-induced cognitive disorders. The aims of this study were to evaluate the effect of alcohol on short-term memory function and histology, and to identify the drug responses and an association with aging process to understand a biological mechanism underlying alcoholic dementia.
Methods : In experiment 1, T-maze tests were done in 5 aged controls and 5 atropine-treated rats. In experiment 2, T-maze tests were repeated on every week for a month in 5 normal adult and 5 ethanol-treated rats. In experiment 3, T-maze tests were repeated on every week for a month in seven groups of 5 ethanol-treated rats injected with normal saline, fluoxetine, bromocriptine, bethacholine, nimodipine, clonidine and ketamine. After completion of behavioral tests, rats were sacrificed by the intracardiac pertusion with phosphate buffered 10% formaldehyde solution, and the brain specimen was stained with hematoxylin-eosin to count cells in prefrontal cortex and hippocampus.
Results : 1)Cell numbers of hippocampus(CA1, CA3 and dentate gyrus) and prefrontal cortex were reduced in ethanol-treated rats(P＜0.05) without significant changes on T-maze tests. 2)Cell numbers of hippocampus(CA1, CA3 and dentate gyrus) and prefrontal cortex were recovered by bethacholine(P＜0.05), while those of hippocampus raised by bromocriptine and clonidine(P＜0.05 respectively). There were no significant changes on T-maze tests. 3)Cell numbers of prefrontal cortex in ethanol-treated rats were correlated with those of atropine-treated(r=0.977, P＜0.001), and of normal aged(r=0.448, P＜0.05) rats.
Conclusions : Alcohol-induced memory disorder might be mainly related with cholinergic system as well as adrenergic or dopaminergic ones. Pathological aging process could be involved in a mechanism underlying alcoholic dementia.
Methods : In experiment 1, T-maze tests were done in 5 aged controls and 5 atropine-treated rats. In experiment 2, T-maze tests were repeated on every week for a month in 5 normal adult and 5 ethanol-treated rats. In experiment 3, T-maze tests were repeated on every week for a month in seven groups of 5 ethanol-treated rats injected with normal saline, fluoxetine, bromocriptine, bethacholine, nimodipine, clonidine and ketamine. After completion of behavioral tests, rats were sacrificed by the intracardiac pertusion with phosphate buffered 10% formaldehyde solution, and the brain specimen was stained with hematoxylin-eosin to count cells in prefrontal cortex and hippocampus.
Results : 1)Cell numbers of hippocampus(CA1, CA3 and dentate gyrus) and prefrontal cortex were reduced in ethanol-treated rats(P＜0.05) without significant changes on T-maze tests. 2)Cell numbers of hippocampus(CA1, CA3 and dentate gyrus) and prefrontal cortex were recovered by bethacholine(P＜0.05), while those of hippocampus raised by bromocriptine and clonidine(P＜0.05 respectively). There were no significant changes on T-maze tests. 3)Cell numbers of prefrontal cortex in ethanol-treated rats were correlated with those of atropine-treated(r=0.977, P＜0.001), and of normal aged(r=0.448, P＜0.05) rats.
Conclusions : Alcohol-induced memory disorder might be mainly related with cholinergic system as well as adrenergic or dopaminergic ones. Pathological aging process could be involved in a mechanism underlying alcoholic dementia.
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