Short-lived diabetes in the young-adult ZDF rat does not exacerbate neuronal Ca(2+) biomarkers of aging.
Short-lived diabetes in the young-adult ZDF rat does not exacerbate neuronal Ca(2+) biomarkers of aging.
复制标题
年轻成年 ZDF 大鼠的短期糖尿病不会加剧衰老的神经元 Ca(2) 生物标志物。
DOI：
10.1016/j.brainres.2014.10.052
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发表时间：
2015
期刊：
影响因子：
2.9
通讯作者：
Thibault,Olivier
中科院分区：
文献类型：
--
作者：
Maimaiti,Shaniya;DeMoll,Chris;Anderson,KatieL;Griggs,RyanB;Taylor,BradleyK;Porter,NadaM;Thibault,Olivier
临床研究结果表明，相对较晚的认知变化可能与糖尿病、肥胖、久坐不动的生活方式和致动脉粥样硬化饮食等先前的疾病有关。因此，2型糖尿病（T2DM）的一些特征可以被认为是衰老的致病因素，有助于年龄依赖性认知能力下降和我们对阿尔茨海默病的易感性。似乎代谢状态的持续时间和个体的年龄都可能对周围和大脑健康产生潜在影响。由于有强有力的证据表明，在动物衰老模型中，Ca2+失调会改变神经元健康、突触可塑性以及学习和记忆过程，我们测试了外周代谢失调可能加剧海马CA1神经元Ca2+功能障碍的假设。利用细胞内/细胞外电生理和Ca2+成像技术，我们发现在休息或突触刺激期间，Ca2+水平、Ca2+依赖性后超极化、基线场电位和短期突触可塑性在年轻成年雄性Zucker糖尿病肥胖大鼠中与瘦大鼠相比没有显着改变。我们的观察表明，在糖尿病动物模型中，以高水平葡萄糖和胰岛素为特征的T2DM早期阶段可能太过短暂，无法改变海马CA1生理。临床数据表明，T2DM病程越长，对认知功能的负面影响越大。这篇文章是《SI：大脑与记忆》特刊的一部分。
Results from clinical studies provide evidence that cognitive changes relatively late in life may be traced to antecedent conditions including diabetes, obesity, a sedentary lifestyle, and an atherogenic diet. As such, several traits of Type 2 diabetes (T2DM) could be considered pathogenic factors of aging, contributing to age-dependent cognitive decline and our susceptibility to Alzheimer‘s disease. It appears that both the duration of metabolic condition and the age of the individual, together can contribute to the potential impact on peripheral as well as brain health. Because of robust evidence that in animal models of aging, Ca2+dysregulation alters neuronal health, synaptic plasticity, and learning and memory processes, we tested the hypothesis that peripheral metabolic dysregulation could exacerbate Ca2+dysfunction in hippocampal CA1 neurons. Using intracellular/ extracellular electrophysiological and Ca2+imaging techniques, we show that Ca2+levels at rest or during synaptic stimulation, the Ca2+-dependent afterhyperpolarization, baseline field potentials, and short-term synaptic plasticity were not significantly altered in young-adult male Zucker diabetic fatty rats compare to their lean counterparts. Our observations suggest that early phases of T2DM characterized by high levels of glucose and insulin may be too transient to alter hippocampal CA1 physiology in this animal model of diabetes. These results are supported by clinical data showing that longer T2DM duration can have greater negative impact on cognitive functions.This article is part of a Special Issue entitled SI: Brain and Memory.