Contestabile Andrea, Ciani Elisabetta, Contestabile Antonio
Department of Human and General Physiology, Bologna, Italy.
Brain Res. 2004 Mar 26;1002(1-2):162-6. doi: 10.1016/j.brainres.2004.01.005.
Reduced caloric intake obtained through long-term dietary restriction has been found beneficial in some animal models of neurodegeneration. We report here that rats maintained under dietary restriction from the second to the eighth month of age are fully protected towards degeneration of GABAergic neurons in the hippocampus and the olfactory-entorhinal cortex caused by systemic administration of the convulsant toxin, kainic acid. However, in a different model of excitotoxic neurodegeneration, injection of ibotenic acid in the forebrain magnocellular basal nucleus, the decrease of a cholinergic marker in the target areas of the cortex was only partially protected by dietary restriction. Thus, in different experimental models neurodegeneration can be differentially rescued by dietary restriction. Analysis of alterations in the expression of relevant genes in different experimental conditions, could help in better understanding these differences.
通过长期饮食限制减少热量摄入已被发现在一些神经退行性疾病的动物模型中有益。我们在此报告,从第二个月到第八个月处于饮食限制下的大鼠,对由全身性给予惊厥毒素 kainic 酸引起的海马体和嗅内嗅皮层中 GABA 能神经元的退化具有完全保护作用。然而,在另一种兴奋性毒性神经退行性疾病模型中,在前脑大细胞基底核注射鹅膏蕈氨酸,饮食限制仅部分保护了皮层靶区域中胆碱能标志物的减少。因此,在不同的实验模型中,饮食限制对神经退行性变的挽救作用可能存在差异。分析不同实验条件下相关基因表达的变化,有助于更好地理解这些差异。