Caloric restriction prevents age-related deficits in LTP and in NMDA receptor expression
Caloric restriction prevents age-related deficits in LTP and in NMDA receptor expression
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DOI：
10.1016/s0169-328x(00)00088-7
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发表时间：
2000-05-31
期刊：
影响因子：
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通讯作者：
Browning, MD
中科院分区：
文献类型：
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作者：
Eckles-Smith, K;Clayton, D;Browning, MD
衰老研究的一个主要焦点是寻找能够预防或改善与衰老相关的记忆缺陷的治疗方法。据报道，一种范例，即终生热量限制，可以减少衰老的一些影响。在当前的报告中，我们研究了这种治疗对与年龄相关的 LTP 缺陷的影响，LTP 是记忆形成的假定细胞组成部分。我们在此报告，终身热量限制可以完全预防与年龄相关的 LTP 缺陷。此外，我们报告说，老年大鼠中 NMDA 受体亚基 NR1 的表达显着下降，这种与年龄相关的缺陷也可以通过热量限制来预防。这些数据提供了一种分子和细胞机制，通过这种机制，终生热量限制可以改善与衰老过程相关的一些认知缺陷。 (C) 2000 年由 Elsevier Science B.V. 出版
A major focus of aging research has been the search for treatments that will prevent or ameliorate the memory deficits associated with aging. One paradigm, lifelong caloric restriction, has been reported to reduce some of the effects of aging. In the current report, we examined the effects of this treatment on age-related deficits in LTP, a putative cellular building block for memory formation. We report here that lifelong caloric restriction completely prevents the age-related deficit in LTP. In addition, we report that there is a dramatic decrease in the expression of the NMDA receptor subunit NR1 in aged rats and this age-related defect is also prevented by caloric restriction. These data provide a molecular and cellular mechanism by which life long caloric restriction may ameliorate some of the cognitive deficits associated with the aging process. (C) 2000 Published by Elsevier Science B.V.